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Minipress (Prazosin)
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Minipress

Minipress is an effective strong preparation which is taken in treatment of hypertension diseases. Minipress is also helpful in treatment of male prostate enlargement symptoms, congestive heart failure, Raynaud's disease. Minipress acts as anti-hypertension remedy.

Other names for this medication:

Similar Products:
Lisinopril, Amlodipine, Norvasc, Benicar, Metoprolol, Hydrochlorothiazide, Avapro, Losartan

 

Also known as:  Prazosin.

Description

Minipress is created by pharmacy specialists to combat hypertension disease. Target of Minipress is to control level of blood pressure.

Minipress acts as anti-hypertension remedy. Minipress operates by reducing blood pressure.

Minipress is also known as Prazosin, Prazopress, Vasoflex, Hypovase.

Minipress is alpha blocker.

Generic name of Minipress is Prazosin (oral).

Brand name of Minipress is Minipress.

Dosage

You should take it by mouth with water.

It is better to take Minipress 2-3 times a day at the same time with meals or milk.

It is better to start the first Minipress dose when are going to bed.

If you want to achieve most effective results do not stop taking Minipress suddenly.

Overdose

If you overdose Minipress and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Minipress overdosage: feeling lightheaded, rash, weakness, troublesome breathing, pruritus, swelling.

Storage

Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture, light and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children in a container that small children cannot open.

Side effects

The most common side effects associated with Minipress are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.

Contraindications

Do not take Minipress if you are allergic to Minipress components.

Be careful with Minipress if you're pregnant or you plan to have a baby, or you are a nursing mother.

Be careful with Minipress if you are taking any prescription or nonprescription medicine, herbal preparation, or dietary supplement.

Be careful with Minipress if you have allergies to medicines, foods, or other substances.

Be careful with Minipress if you have liver or kidney disease, heart failure, low blood pressure, narcolepsy, prostate cancer.

Be careful with Minipress if you take muscle relaxants as carisoprodol; anti-anxiety drugs as diazepam; anti-seizure drugs as carbamazepine; tranquilizers; sleep medicines as sedatives; antihistamines as diphenhydramine; verapamil; psychiatric medicines as tricyclic antidepressants (amitriptyline), phenothiazines (chlorpromazine); sexual function problems drugs as vardenafil, sildenafil, tadalafil; narcotic pain relievers as codeine; beta blockers as metoprolol, propranolol, atenolol.

Avoid machine driving.

Use Minipress with great care in case you want to undergo an operation (dental or any other).

Avoid alcohol.

Minipress can be not safety for elderly people.

Try to be careful with sunbeams. Minipress makes skin sensitive to sunlight. Protect skin from the sun.

Do not stop taking Minipress suddenly.

minipress xl dose

Predominance in the urethra and prostate of the alpha(1A)-adrenoceptor subtype, which is believed to be the receptor mediating noradrenaline induced smooth muscle contraction in these tissues, led to the preparation of alpha(1A)-selective antagonists to be tested as uroselective compounds for the treatment of benign prostatic hyperplasia. Thus, a number of selective alpha(1A)-adrenoceptor antagonists were synthesized and assayed in vitro for potency and selectivity. Dog pharmacokinetic parameters of 12 (RO700004) and its metabolite 40 (RO1104253) were established. The relative selectivity of intravenously administered 12, 40 and standard prazosin to inhibit hypogastric nerve stimulation-induced increases in intraurethral prostatic pressure versus phenylephrine-induced increases in diastolic blood pressure in anesthetized dogs was 76, 71 and 0.6, respectively.

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After treatment, there were 5 cured cases, 13 markedly effective cases, 9 effective cases, 1 ineffective case, and 2 eliminated cases in the experimental group, as compared with 2 cured cases, 8 markedly effective cases, 10 effective cases, 7 ineffective cases, and 3 eliminated cases in the control group. The total effectiveness rate was obviously higher in the former (96.4%) than in the latter (74.1%). IPSS, Qmax, and CSS were improved in both of the groups after medication, even more significantly in the experimental than in the control group (IPSS: 15.22 ± 2.98 vs 18.15 ± 5.88, P <0.05; Qmax: [13.56 ± 2.26] ml/s vs [11.78 ± 2.97] ml/s, P <0.05; CSS: 6.18 ± 2.13 vs 9.52 ± 3.15, P <0.05). Because of the difference in the QOL score between the two groups at the baseline (P = 0.038 <0.05), no more comparison was made in this aspect after treatment.

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Losartan, an AT1 angiotensin II (ANG II) receptor non-peptide antagonist, induces an increase in mean arterial pressure (MAP) when injected intracerebroventricularly (icv) into rats. The present study investigated possible effector mechanisms of the increase in MAP induced by icv losartan in unanesthetized rats. Male Holtzman rats (280-300 g, N = 6/group) with a cannula implanted into the anterior ventral third ventricle received an icv injection of losartan (90 micro g/2 micro l) that induced a typical peak pressor response within 5 min. In one group of animals, this response to icv losartan was completely reduced from 18 +/- 1 to 4 +/- 2 mmHg by intravenous (iv) injection of losartan (2.5-10 mg/kg), and in another group, it was partially reduced from 18 +/- 3 to 11 +/- 2 mmHg by iv prazosin (0.1-1.0 mg/kg), an alpha1-adrenergic antagonist (P<0.05). Captopril (10 mg/kg), a converting enzyme inhibitor, injected iv in a third group inhibited the pressor response to icv losartan from 24 +/- 3 to 7 +/- 2 mmHg (P<0.05). Propranolol (10 mg/kg), a beta-adrenoceptor antagonist, injected iv in a fourth group did not alter the pressor response to icv losartan. Plasma renin activity and serum angiotensin-converting enzyme activity were not altered by icv losartan in other animals. The results suggest that the pressor effect of icv losartan depends on angiotensinergic and alpha1-adrenoceptor activation, but not on increased circulating ANG II.

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Matrix-assisted laser desorption/ionisation time-of-flight mass spectrometry (MALDI-TOFMS) has been investigated as a tool for accurate determination of the molecular mass of synthetic analogues of prazosine, a molecule used for the treatment of hypertension. Samples were dissolved in methanol, mixed with mass calibration standards, and crystallised on the target with alpha-cyano-4-hydroxycinnamic acid as matrix. Acquisition of spectra was rapidly completed in reflectron mode, allowing high resolution (6000-10000) and sensitive (about 1-10 pmol of sample on target) determination of the synthetic products. The results show the effectiveness of MALDI-TOFMS for accurate mass determination of these fairly large molecules, which are otherwise difficult to analyse by other high-resolution mass spectrometric techniques.

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After bilateral superior cervical ganglionectomy (SCGx) of adult male rats, norepinephrine (NE) content of the medial basal hypothalamus (MBH) decreased significantly by 39-47% from 16 h to 7 days after surgery. During this time the levels of serum growth hormone (GH) and prolactin (PRL) and of MBH GH-releasing hormone (GRH), thyrotropin-releasing hormone (TRH) and somatostatin were measured by RIA. In sham-operated controls, serum PRL increased and serum GH decreased 16-24 h after surgery, attaining pre-surgical levels later on. In SCGx rats, significantly lower serum GH and PRL and higher MBH GRH and TRH content as compared to controls was observed 16-24 h after surgery, during the wallerian degeneration phase after SCGx. MBH somatostatin concentration decreased in SCGx rats 20 h after surgery. Two injections of the alpha 1-adrenoceptor blocker prazosin 45 and 90 min before sacrifice, alone or together with the beta-blocker propranolol, prevented the changes in MBH hypophysiotropic hormone content, as well as in serum GH and PRL levels, found in SCGx rats 20 h after surgery. Propranolol treatment did not affect hormone levels. Neither drug modified the decrease in MBH NE content observed after SCGx. The results argue in favor of the existence of physiologically relevant projections from superior cervical ganglion neurons to the MBH controlling hypophysiotropic hormone release.

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After a 2-year combination therapy, discontinuation of either one drug induced benign prostatic hyperplasia progression in either group. Greater risk of resuming medication and needing TURP were noted in patients who discontinued 5ARI.

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We have synthesized and examined some of the pharmacological properties of 6-[N,S-dimethyl-N'-cyanoisothioureidomethyl]-6,11-dihydro-5H- dibenz(b,e)azepine hydrochloride (Fran 12), a derivative of 6-methylaminomethyl-6,11-dihydro-5H- dibenz[b,e,]azepine. In the guinea-pig isolated ileum, Fran 12 (10(-7)-10(-5) M) caused parallel rightward shifts of the concentration-response curves to histamine. A Schild plot gave a pA2 of 7.48, with a slope not significantly different from -1.0. In the rat stomach fundus strip and in endothelium-denuded aortic rings, Fran 12 inhibited contractile responses to 5-hydroxytryptamine in a non-competitive manner. In both chloralose-anaesthetized and pithed rats, it inhibited pressor responses to 5-hydroxytryptamine. It had no effect on depressor responses to 5-hydroxytryptamine in anaesthetized rats. In pithed rats, Fran 12 (0.25-2 mg/kg, i.v.) produced dose-dependent increases in blood pressure. These were not inhibited by i.v. phentolamine, prazosin, yohimbine, propranolol, methysergide, pentolinium or atropine but were inhibited by verapamil. These results indicate that Fran 12 is a histamine and 5-hydroxytryptamine antagonist which also exerts pressor effects via a peripheral action. The pressor action does not appear to be mediated via effects on alpha 1- or alpha 2-adrenoceptors, muscarinic or nicotinic cholinoceptors or 5-hydroxytryptamine receptors, although calcium channel activation may play a role.

minipress drug class

The induction of complex bilateral leg muscle activation combined with coordinated stepping movements is demonstrated in patients with complete paraplegia. This was achieved by partially unloading patients who were on a moving treadmill. In comparison to healthy subjects, the paraplegic patients displayed a less dynamic mode of muscle activation. In all other respects leg muscle electromyographic activity was modulated in a similar manner to that in healthy subjects. However, the level of electromyographic activity in the gastrocnemius (the main antigravity muscle during gait) was considerably lower in the patients. During the course of a daily locomotor training program, the amplitude of gastrocnemius electromyographic activity increased significantly during the stance phase, while inappropriate tibialis anterior activation decreased. Incompletely paraplegic patients benefited from the training with respect to performance of unsupported stepping movements on solid ground. In about half of completely paraplegic patients with low muscle tone, no beneficial effect of the training was seen. This may be due to an inhibitory effect on spinal neuronal activity by drugs patients were taking (e.g., prazosin, clonidine, cannabinoids). In this study intrathecal application of clonidine drastically reduced, while epinephrine enhanced locomotor muscle electromyographic activity. The results of this study promise to be significant in the treatment of paraplegic patients.

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Long-term treatment with (±)doxazosin produces potent hypotensive action in conscious rats that seems to result from synergic interaction of the two enantiomers.

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To explore the efficacy of levofloxacin, terazosin, and their combination in patients with category III chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS).

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Methamphetamine (2-15 mg/kg, i.p.) has been shown to induce interleukin-1 beta (IL-1 beta) mRNA in the rat hypothalamus. The induction of IL-1 beta mRNA was blocked by intraperitoneal pretreatment with beta-blockers propranolol (0.1-1 mg/kg, but not 0.01 mg/kg) and pindolol (0.3 and 1 mg/kg). Prazosin (1 and 5 mg/kg) and yohimbine (1 and 5 mg/kg), alpha-blockers and haloperidol (1 mg/kg), a dopamine antagonist, produced partial and little suppression, respectively. When injected intracerebroventricularly (i.c.v.), propranolol, but neither prazosin nor yohimbine, significantly suppressed the methamphetamine-induced expression of IL-1 beta mRNA at a dose of 1 nmol/rat. An i.c.v. injection of the beta-adrenoceptor agonist isoproterenol (1 and 3 micrograms/rat) dose-dependently increased the hypothalamic level of IL-1 beta mRNA. The present results suggest that the induction of hypothalamic IL-1 beta mRNA by methamphetamine is mediated by beta-adrenoceptors in the brain.

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Nerve terminals obtained from rat brain cortex and hippocampus, were labelled with 0.04 microM of [3H]noradrenaline ([3H]NA). Thereafter the basal release of [3H]NA was measured in a Brandel superfusion apparatus, in the presence of alpha 1-adrenoceptor agonists (phenylephrine or noradrenaline) or these alpha 1-adrenoceptor agonists along with prazosin, an alpha 1-adrenoceptor antagonist. In cortical synaptosomes both alpha 1-adrenoceptor agonists increased the basal release of [3H]NA in a concentration-dependent manner (EC50 = 0.15 microM for phenylephrine and 12.6 microM for noradrenaline). Effects were reversed by 0.01 microM prazosin (EC50 = 2.46 and 130.1 microM, respectively). In synaptosomes from rat brain hippocampus, phenylephrine (EC50 = 1.28 microM) and noradrenaline (EC50 = 33.7 microM) also increased the [3H]NA release and prazosin (0.01 microM) shifted the corresponding concentration-response curves to the right (EC50 = 7.38 and 264.0 microM, respectively). Events produced by noradrenaline acting as alpha 1-adrenoceptor agonist did not show Ca2+ dependence. These results suggest (1) the presence of functional alpha 1-adrenoceptors in nerve terminals from rat brain cortex and hippocampus, (2) that these receptors seem to play a role in the presynaptic modulation of [3H]NA release, and (3) that intraterminal Ca2+ may be involved.

minipress drug interactions

Canine uterine arteries are innervated by adrenergic, vasoconstrictor and nitroxidergic vasodilator nerves, and the neurogenic vasodilation is evidently more marked than that in other canine arteries, including the iliac artery.

minipress drug information

After 4 years, women who were randomized to lifestyle intervention only were less likely to be receiving step 1 therapy alone (placebo) than men who were randomized to placebo therapy (46% vs 66%, respectively, P < .01). There were significantly greater decreases in the mean systolic blood pressure in both men and women who were assigned to treatment with active drugs compared with those participants who were receiving placebo therapy; differences among treatments with active drugs were similar between men and women. Men experienced larger falls in their total and low-density lipoprotein cholesterol and triglyceride levels regardless of the treatment assignment than did women; however, there were no significant sex-by-treatment interactions. Quality-of-life indexes were generally improved with active drug treatment compared with placebo therapy in both sexes; there was a sex-by-treatment interaction for the general health index. The relative risk (RR) for combined clinical events was similar in women (RR, 0.64; 95% confidence interval [CI], (0.36 to 1.16) and in men (RR, 0.67; 95% CI, 0.40 to 1.14) who were assigned to treatment with all active drugs combined, compared with those who were receiving placebo therapy.

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This study investigated mechanisms involved in the maintenance of the functional response pattern of the postjunctional alpha(1)-adrenoceptor in vas deferens isolated from rats submitted to acute swimming stress. The plasma corticosterone levels increased approximately three times after the swimming stress in the nontreated rats as well as after swimming stress in the rats pretreated with desipramine (DMI), yohimbine (YO), or DMI with YO. No alteration was detected in the sensitivity to norepinephrine (NE) in the vasa deferentia from the stressed rats or stressed rats treated with DMI or DMI with YO, in relation to their respective control. However, when the vasa deferentia were previously incubated with DMI, a reduction in sensitivity to NE in organs from stressed rats was observed. Vasa deferentia excised from rats pretreated with YO before the swimming stress showed an increase in postjunctional alpha(1)-response that was abolished by prazosin (PZ). Thus, the neuronal uptake, the prejunctional alpha(2)-adrenoceptors (mediating prejunctional inhibition), the occupancy and functional response of the postjunctional alpha(1)-adrenoceptors, and the emotional stress component were very important for the determination of the noradrenergic response pattern in vas deferens from rats submitted to acute swimming stress.

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Vasoconstriction of carotid arteriovenous anastomoses may be involved in the therapeutic action of acutely acting anti-migraine agents, including the triptans and ergot alkaloids. While 5-HT1B/1D receptors mediate the effect of triptans, ergotamine and dihydroergotamine also interact with alpha-adrenoceptors. In the present study, we investigated the potential role of alpha1- and alpha2-adrenoceptors in mediating vasoconstriction of carotid arteriovenous anastomoses in anaesthetized pigs. Ten minute intracarotid infusions of phenylephrine (1, 3 and 10 microg kg(-1) min(-1)) or BHT 933 (3, 10 and 30 microg kg(-1) min(-1)) produced dose-dependent decreases in total carotid and arteriovenous anastomotic conductances; no changes were observed in the capillary fraction. The carotid vascular effects of phenylephrine and BHT 933 were selectively abolished by prazosin (100 microg kg(-1), i.v.) and rauwolscine (300 microg kg(-1), i.v.), respectively. The responses to phenylephrine and BHT 933 were not affected by the selective 5-HT1B/1D receptor antagonist GR127935 (500 microg kg(-1), i.v.). These results show that both alpha1- and alpha2-adrenoceptors can mediate vasoconstriction of carotid arteriovenous anastomoses in anaesthetized pigs. Since vasoconstrictor activity in this in vivo model is predictive of anti-migraine activity, an agonist activity at particularly the alpha2-adrenoceptor subtypes, in view of their less ubiquitous nature, could provide migraine abortive potential. Thus, the present results may aid further understanding of the mode of action of some current anti-migraine agents and may eventually be helpful in the development of future treatment in migraine.

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A prejunctional mechanism involving an alpha 1-adrenergic receptor may exert control on the release of acetylcholine from parasympathetic nerve endings in the heart. To test this hypothesis in vivo, rats were prepared for electrical stimulation of the vagus nerves. Blood pressures and heart rates were monitored, and the animals were treated with alpha-agonists and alpha-antagonists. The alpha 1-selective agonist phenylephrine significantly attenuated vagally induced bradycardia in a dose-dependent fashion (ED50 = 19 micrograms/kg). This is consistent with the hypothesis that there is alpha-adrenergic inhibition of ACh release. In contrast, the alpha 2-selective agonist, BHT-920, caused no change in heart rate during vagal stimulation. The effects of phenylephrine to raise heart rate and blood pressure during vagal stimulation were blocked by the alpha 1-selective antagonist prazosin (ID50 approximately 1 microgram/kg) but not by the alpha 2-selective antagonists yohimbine and rauwolscine. This further supports an alpha 1 assignment to the prejunctional adrenergic receptor mechanism, which can regulate the release of acetylcholine from cardiac parasympathetic neurons.

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The effects of prazosin HCl treatment on several variables were determined in 16 patients suffering from micturition disturbances associated with benign prostatic hypertrophy. After administration of the drug in doses of 1-2 mg/day, subjective symptoms improved in 11 patients (68.8%). Urine retention rate, maximum urine flow rate, and average urine flow rate exhibited statistically significant improvement, but voided urine volume did not. Urethral pressures declined significantly in the bladder neck and prostatic urethra but not in the pressure at the external sphincter. The results suggest prazosin HCl may be effective in small doses in symptomatic treatment of benign prostatic hypertrophy.

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The present study evaluated the effects of melatonin on the discharge rate of tonically active medial vestibular nucleus (MVN) neurons in an in vitro slice preparation of the rat dorsal brainstem. The results demonstrated that, when melatonin was applied to the slice for a period of 7-10 min, a decrease in MVN neuron firing rate was observed in 21/58 (36%) of the cells sampled. The inhibitory effects of melatonin were present in synaptic uncoupling condition and were mimicked by 2-iodomelatonin, a non-selective agonist with high affinity for melatonin membrane receptor subtypes (MT(1), MT(2), MT(3)). The MT(2) receptor antagonists luzindole and 4-phenyl-2-propionamidotetraline and the MT(3) receptor antagonist prazosin did not, however, antagonise the inhibitory effects of melatonin, indicating that melatonin may act on MVN neurons through an MT(1) receptor-mediated mechanism.

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Pinacidil is an orally administered antihypertensive drug that acts via direct relaxation of vascular smooth muscle to produce peripheral vasodilatation and a reduction in blood pressure without significant direct effects on cardiac electrophysiology. Pinacidil is unrelated to other antihypertensive drugs in clinical use, either in structure or mechanism of action. It belongs to a new class of agents called 'potassium channel openers' which act via potassium efflux to hyperpolarize cell membranes, indirectly causing a net reduction in intracellular calcium that leads to relaxation of vascular smooth muscle. Pinacidil is indicated in the management of essential hypertension. In clinical trials of up to 1 year duration, pinacidil administered twice daily in a controlled release capsule formulation has been shown to achieve adequate blood pressure control both in previously untreated patients and in those with blood pressure inadequately controlled by beta-adrenoceptor blocking drugs or thiazide diuretics. In long term (up to 1 year) comparative studies pinacidil was at least as effective as hydralazine, prazosin or nifedipine in maintaining blood pressure control. Pinacidil may also have a potential use in the treatment of patients with secondary renal hypertension. Clinical trials to date have usually allowed the addition of a thiazide diuretic and/or beta-adrenoceptor blocking drug to enhance the efficacy of pinacidil and/or to reduce the incidence of adverse effects. The main adverse effects of pinacidil treatment, which result from its peripheral vasodilator activity, are headache, oedema, palpitations and tachycardia. Although the overall incidence of adverse effects is quite high, they are usually mild, transient in nature and respond to a reduction in dose. Nevertheless, these effects may occasionally be severe, necessitating withdrawal from therapy. Thus, pinacidil is an effective antihypertensive drug for the treatment of mild to moderate essential hypertension. Despite its novel mechanism of action pinacidil causes adverse effects typical of peripheral vasodilators; during long term use with twice daily administration of the controlled release capsule formulation, the addition of a diuretic is often necessary to attenuate peripheral oedema and maintain adequate control of blood pressure. Further long term controlled trials are needed to determine the precise role of pinacidil relative to that of the angiotensin converting enzyme (ACE) inhibitors and calcium channel blocking drugs.

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minipress 1mg tablet 2016-06-01

Subtypes of alpha1-adrenoceptor in rabbit iris have been examined in functional, binding and molecular biological experiments. In functional studies, exogenous and endogenous noradrenaline produced contractions of the iris dilator muscle. The contractile responses to noradrenaline were competitively antagonized by a range of alpha1-adrenoceptor antagonists (pA2 values): prazosin (8.1), WB4101 (8.2), BMY7378 (5.9), YM617 (9.5), JTH-601 (8.8), HV723 (7.8) and KMD-3213 (9.8). The same order of inhibitory potency was seen in the adrenergic responses to electrical stimulation. This affinity profile corresponds well to that of the putative alpha1L-adrenoceptor, which has been proposed in lower urinary tract tissues. In binding studies on rabbit iris membrane however, prazosin, KMD-3213 and WB4101 displayed high affinity (pKd or pKi: 9.6, 10.3, 9.6, respectively), and BMY7378 displayed low affinity (pKi: 6.9). These results show that the binding sites typically correspond to alpha1A-adrenoceptor subtype in character, and we could not buy minipress online detect the significant amount of alpha1L-adrenoceptor subtype. The expression of the three distinct mRNAs that encode proteins of alpha1a-, alpha1b- and alpha1d-adrenoceptors was studied using reverse transcription-polymerase chain reaction (RT-PCR). RT-PCR demonstrated the strongest expression of the alpha1a-adrenoceptor, weak expression of the alpha1b-adrenoceptor and undetectable expression of the alpha1d-adrenoceptor. The present study suggests that alpha1A-adrenoceptor is a major subtype detectable in binding and RT-PCR studies in rabbit iris, but that the adrenergic contractions of iris dilator muscle are mediated via activation of alpha1-adrenoceptor subtype having low affinity for prazosin and WB4101.

minipress medicine 2016-12-17

The effects of prazosin treatment on blood pressure and diabetic control were assessed in 22 patients with stable non-insulin-dependent diabetes mellitus and hypertension. After an initial six-week baseline period, patients were titrated to optimal therapeutic doses of prazosin (mean daily dose, 12.9 +/- 6.5 mg). Both sitting and standing systolic and diastolic blood pressures were significantly decreased (p = 0.01) with prazosin therapy from a mean of 152/99 mm Hg sitting and 144/99 mm Hg standing to a mean of 139/84 mm Hg and 133/85 mm Hg, respectively, at the end of titration and throughout the buy minipress online 12-week prazosin maintenance therapy period. Seventy-seven percent of patients achieved the goal sitting diastolic blood pressure of 85 mm Hg or less. Total cholesterol, high-density lipoprotein cholesterol, and triglyceride levels were not significantly altered during prazosin therapy compared with baseline measurements. Diabetic control and renal function were maintained during prazosin treatment with no significant changes from baseline noted. No unexpected adverse experiences were reported. In summary, prazosin treatment effectively reduced blood pressure without compromising diabetic control or renal function in this group of hypertensive patients with concomitant diabetes mellitus.

minipress xl drug 2015-02-15

1. Several alpha 1- and alpha 2-adrenoceptor agonists and antagonists were examined for effects on spontaneous and stimulus-evoked release of [3H]noradrenaline from sympathetic nerves in guinea-pig vas deferens. 2. Prazosin (0.1 and 1 microM), phentolamine (30 microM) and yohimbine (10 microM) each enhanced the stimulus-evoked release of [3H]noradrenaline. 3. Prazosin and phentolamine increased buy minipress online the spontaneous outflow of [3H]noradrenaline, whereas yohimbine was without effect. 4. Methoxamine (10 microM) and clonidine (0.1 microM) inhibited the stimulus-evoked release of [3H]noradrenaline, whereas only methoxamine (1 microM) decreased the spontaneous outflow of [3H]noradrenaline. 5. The identity of prejunctional alpha-adrenoceptors in the guinea-pig vas deferens is discussed.

minipress 2 mg 2017-02-22

The median preoptic nucleus (MnPO) in the lamina terminalis receives a prominent catecholaminergic innervation from the dorsomedial and ventrolateral medulla. The present investigation used whole cell patch-clamp recordings in rat brain slice preparations to evaluate the hypothesis that presynaptic adrenoceptors could modulate GABAergic inputs to MnPO neurons. Bath applications of norepinephrine (NE; 20-50 microM) induced buy minipress online a prolonged and reversible suppression of inhibitory postsynaptic currents (IPSCs) and reduced paired-pulse depression evoked by stimulation in the subfornical organ and organum vasculosum lamina terminalis. These events were not correlated with any observed changes in membrane conductance arising from NE activity at postsynaptic alpha(1)- or alpha(2)-adrenoceptors. Consistent with a role for presynaptic alpha(2)-adrenoceptors, responses were selectively mimicked by an alpha(2)-adrenoceptor agonist (UK-14304) and blockable with an alpha(2)-adrenoceptor antagonist (idazoxan). Although the alpha(1)-adrenoceptor agonist cirazoline and the alpha(1)-adrenoceptor antagonist prazosin were without effect on these evoked IPSCs, NE was noted to increase (via alpha(1)-adrenoceptors) or decrease (via alpha(2)-adrenoceptors) the frequency of spontaneous and tetrodotoxin-resistant miniature IPSCs. Collectively, these observations imply that both presynaptic and postsynaptic alpha(1)- and alpha(2)-adrenoceptors in MnPO are capable of selective modulation of rapid GABA(A) receptor-mediated inhibitory synaptic transmission along the lamina terminalis and therefore likely to exert a prominent influence in regulating cell excitability within the MnPO.

minipress drug information 2016-04-09

Presence of charge on the cyclodextrin structure provides an additional site of interaction compared to neutral cyclodextrins, which may be modified using buy minipress online solution ionic strength.

tab minipress dosage 2016-12-19

Imipramine is a tricyclic antidepressant inhibitor of norepinephrine and serotonin neuronal reuptake. The roles of specific α1-adrenoceptor subtypes that might be targeted by the increased synaptic levels of noradrenaline induced by imipramine are not well understood. This study investigates the α1-adrenoceptor subtypes involved in the anti-immobility effect of imipramine in the mouse tail suspension test. The anti-immobility effect of imipramine (32mg/kg, i.p.) was significantly antagonised by the non-subtype-selective α1-adrenoceptor antagonist prazosin (0.5 and 1.0mg/kg, i.p.). Neither the selective α1A-adrenoceptor antagonist 5-methyl-3-[3-[3-[4-[2-(2,2,2,-trifluroethoxy)phenyl]-1-piperazinyl]propyl]-2,4-(1H,3H)-pyrimidinedione (RS-100329, 0.5 and 1.0mg/kg) nor the buy minipress online selective α1D-adrenoceptor antagonist 8-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-8-azaspiro[4.5]decane-7,9-dione dihydrochloride, (BMY-7378, up to 1.0mg/kg, i.p.) affected the anti-immobility effect of imipramine. However, the anti-immobility effect of imipramine was significantly antagonised by the selective α1B-adrenoceptor antagonist (2S)-4-(4-amino-6,7-dimethoxy-2-quinazolinyl)-2-[[(1,1-dimethylethyl)amino]carbonyl]-1-piperazinecarboxylate (L-765,314). In addition, mice treated only with RS-100329 or BMY-7378, but not with L-765,314, showed reduced immobility times in comparison to mice treated with vehicle. These results indicate that the selective antagonism of α1A- and α1D-adrenoceptors results in antidepressant-like effects and that the α1B-subtype is the main target for the increased levels of noradrenaline caused by imipramine.

minipress 1mg capsule 2015-10-21

Ten dogs with a 1-month-old anterior wall myocardial infarction were studied. These dogs had all developed, in control conditions, VF during a 2-minute occlusion of the circumflex coronary artery while exercising (n = 9) or lying on the table (n = 1). Afterwards, the dogs underwent additional tests with the following intravenously administered drugs: abanoquil (n = 10; 1 micrograms/kg), prazosin (n = 9; 0.1 mg/kg), and propranolol (n = 10; 1 mg/kg). Internal control analysis was used buy minipress online . All dogs tested had recurrence of VF with both alpha-adrenergic blockers. Propranolol significantly reduced heart rate during ischemia and prevented VF in 5 of 10 dogs tested (P < 0.05). When heart rate was kept constant by atrial pacing (n = 3), 2 of the 3 animals remained protected by propranolol. Just prior to onset of VF, heart rate was not significantly different in the control and in the abanoquil tests (237 +/- 45 and 253 +/- 34 beats/min, respectively), whereas it was higher (P < 0.05) with prazosin (288 +/- 40 beats/min).

minipress tablets dose 2017-05-19

1 Prolonged exposure (6-12 h) of rat aorta to alpha1-adrenergic receptor (alpha(1)AR) agonist phenylephrine (Phe) leads to a decrease in alpha(1)AR-mediated vasoconstriction. This reduced responsiveness to alpha(1)AR stimulation was strongly dependent on the intactness of the endothelium. 2 We examined the effect of Phe on nitric oxide synthase (NOS) activity by measuring the conversion of [(3)H]L-arginine to [(3)H]L-citrulline in rat aorta or in endothelial cells isolated from rat aorta. Phe stimulation increased NOS activity in control aortas. This response was antagonized by prazosin. However, Phe increased neither the activity of NOS nor intracellular Ca(2+) in the isolated endothelial cells from the control aortas, whereas acetylcholine (Ach) was able to stimulate both responses in these cells. This result suggests that Phe stimulates alpha(1)AR on vascular smooth muscle cells and has an indirect influence on endothelial cells to increase NOS activity. 3 In Phe-exposed aortic rings, basal NOS activity was found to have increased compared to vehicle-exposed control rings. Stimulation with Phe or Ach caused a small increase over basal NOS activity in these preparations. Prolonged exposure to Phe also caused an enhancement of Ach-mediated vasorelaxation in rat aorta. 4 Immunoblot and reverse transcription-polymerase chain reaction experiments showed that prolonged exposure of rat aorta to Phe resulted in an increased expression of eNOS, but not iNOS. This increase was antagonized by nonselective antagonist prazosin. Immunohistochemical staining experiments also showed that expression of eNOS increased in endothelial cells after Phe exposure of the aortas. 5 These results, all together, showed that prolonged exposure of rat aorta to alpha(l)AR agonist Phe enhanced the expression of eNOS and basal NOS activity, which probably causes a decreased vasocontractile response to buy minipress online Phe or to other agonists such as 5HT (5-hydroxytryptamine) in rat aorta. 6 This phenomenon can be considered more as a functional antagonism of vasocontractile response to agonists mediated by endothelium than a specific desensitization of alpha(1)AR-mediated signalling in vascular smooth muscle cells.

minipress reviews 2016-10-29

The efficacy and tolerability of doxazosin and atenolol in the management of mild and moderate hypertension were compared in a multicentre, parallel study, the first year of which was randomized and double-blind. Patients who completed this first year were invited to enter a two-year extension phase; the results after the first year are presented. A total of 228 patients entered the double-blind phase (118 received atenolol). A reduction in dose was required by 4% in each group; eight patients on doxazosin and 11 on atenolol were withdrawn due to adverse effects. Ninety-three of the 100 doxazosin patients and 88 of the 104 atenolol patients who completed the double-blind phase agreed to participate in the open extension study. At 24 months, the mean dose of doxazosin was 5.2 mg/day, and of atenolol 66.7 mg/day. From baseline levels of BP of 158/104 mmHg in the doxazosin group and 161/103 mmHg in the atenolol group, average reductions at 24 months were -16/-14 and -19/-15 mmHg respectively. Neither drug had a significant effect on total cholesterol levels. At all four points of measurement over the two years, doxazosin decreased blood triglyceride levels and increased high density lipoprotein (HDL) cholesterol and the HDL: total cholesterol ratio. Atenolol had the opposite effect on buy minipress online each of these lipid values with the differences between the treatment groups being significant. Doxazosin was well tolerated and was shown to be effective as monotherapy in mild and moderate hypertension. Its effect on blood lipids was potentially favourable, and it should therefore be regarded as an alternative first-line drug in hypertensive patients.

minipress 6 mg 2016-05-21

The findings suggest that metoprolol buy minipress online and prazosin treatments reduce the minimal vascular resistance similarly, despite different reductions in blood pressure. Prazosin treatment might also reduce the forearm sympathetic nerve activity. Reductions in minimal forearm vascular resistance during antihypertensive therapy need not be related only to the lowering of the blood pressure per se.

minipress xl tablets 2016-09-26

We examined the effect of one year of treatment with the selective alpha 1-adrenergic inhibitor doxazosin on right ventricular mass (RV mass), left ventricular mass (LV mass), and arterial blood gases. The subjects were 24 outpatients (18 men and 6 women, mean age 68.3 +/- 9.4 years) with chronic pulmonary disease complicated by hypertension who were clinically stable. One year of drug therapy was associated with significant decreases both in systolic pressure (159 +/- 15.2 vs 125.8 +/- 14.1 mmHg, p < 0.05, n = 24), and in LV mass index (101.0 +/- 13.4 vs 97.6 +/- 11.8 gm-2, p < 0.05), n = 24). We obtained the RV mass index by multiplying the thallium score RV/LV count and the LV mass index obtained by echocardiography. One year of drug therapy was associated with a significant increase in RV mass buy minipress online index (42.9 +/- 31.2 vs 53.6 +/- 30.5 gm-2, p < 0.05, n = 8). Vital capacity decreased (2.18 +/- 1.95 vs 1.95 +/- 0.57 l, p < 0.05, n = 24), but PaO2 improved (77.3 +/- 17.2 vs 82.2 +/- 2.4 mmHg, p < 0.05, n = 24). These data indicate that doxazosin can decrease blood pressure and can depress the left ventricle with no adverse effect on oxygenation in patients with chronic pulmonary disease complicated by hypertension. The worsening of RV hypertrophy may have been caused by a mechanism different from the one that caused LV hypertrophy, and by an increase in the work load on the right ventricles secondary to lung deterioration.

minipress drug interactions 2017-07-06

We buy minipress online studied the effects of angiotensin (Ang) I and II in a variety of isolated human cardiac tissues contracting under physiological conditions (37 degrees C, 60 beats.min-1). Ang I and II consistently increased the peak developed force of human atrial muscles by 30-40%, an effect that was completely blocked by 10(-6) M saralasine, but not by the combination of prazosin and propranolol. However, neither Ang I or II had significant inotropic effects in right and left ventricular human preparations. We were also able to demonstrate that the positive inotropic effect of Ang II in human right atrial tissue is mediated by the AT1 receptor subtype but not the AT2 receptor subtype.

minipress user reviews 2017-05-26

Transient outward K+ current was measured using the whole-cell configuration of Geodon Maximum Dose the patch-clamp technique. Myocytes were isolated from the right ventricle of healthy and streptozotocin-induced diabetic rats.

minipress overdose death 2017-11-13

Nicotinic cholinergic receptors mediate autonomic transmission at ganglia. However, whether different subtypes of nicotinic cholinergic receptors expressed in autonomic ganglia elicit distinct roles in mediating sympathetic and parasympathetic regulations remain to be defined. In this study, we observed that different subtypes of nicotinic receptors were responsible for the sympathetic and parasympathetic cardiovascular responses. In urethane anesthetized mice, intravenous injection with cytisine, a non-selective nicotinic agonist, induced a brief but pronounced decrease Pamelor 25mg Capsule in heart rate, followed by increases in heart rate and arterial blood pressure. The bradycardic response was blocked by atropine, and the pressor response was blocked by prazosin, confirming that these responses were parasympathetic and sympathetic activities, respectively. Hexamethonium, a ganglionic blocker, blocked both sympathetic and parasympathetic responses. Pretreatment with methyllycaconitine citrate, a selective alpha7 nicotinic receptor antagonist, significantly attenuated cytisine-induced sympathetic response with little effect on the parasympathetic response. In contrast, pretreatment with dihydro-beta-erythroidine hydrobromide, a selective alpha4beta2 nicotinic receptor antagonist, blocked cytisine-induced parasympathetic response but not the sympathetic response. Pretreatment with dihydro-beta-erythroidine hydrobromide also blocked baroreflex associated parasympathetic bradycardic response. Moreover, treatment with nicotine induced a bradycardic response without a significant pressor response, which was also attenuated by dihydro-beta-erythroidine hydrobromide. Collectively, these data suggest that different nicotinic receptors play distinct roles in sympathetic and parasympathetic ganglia. Specifically, activations of alpha7 and alpha4beta2 nicotinic receptors are involved in cytisine-induced cardiovascular sympathetic and parasympathetic responses, respectively.

minipress dosage forms 2016-11-18

Incidence of orthostatic hypertension is estimated at 5% but is even more prevalent in borderline hypertension and autonomic neuropathies. The aim of this study was to develop a potential model to investigate orthostatic hypertension. We used normotensive and hypertensive Wistar rats to analyze responses and diurnal variations of arterial blood pressure, heart rate, temperature, and locomotor activity by telemetry. Orthostatic tests were carried out during 45 degrees head-up tilt (R, repeated 3 times for 5 minutes; or S, sustained for 120 minutes). Hypertension was induced by blockade of nitric oxide synthesis. In normotensives, horizontal control blood pressure was R115.4 +/- 1.4/S113.7 +/- 1.6 mm Hg and heart rate R386.4 +/- 7.0/S377.9 +/- 8.8 bpm. Head-up tilt increased blood pressure by R4.5/S8.4 mm Hg, including a 3.8 mm Hg hydrostatic component. The sustained hypertensive response was prevented by prazosin (10 mg/kgbw) and augmented by a subanesthetic dose of chloralose (26 mg/kgbw). In NO-deprived hypertension, horizontal control blood pressure and heart rate were R138.4 +/- 2.6/S140.3 +/- 2.7 mm Hg and R342.1 +/- 12.0/S346.0 +/- 8.3 bpm, respectively. Tilt increased blood pressure further by R4.2/S9.4 mm Hg. In both normo- and hypertensives, variables exhibited similar diurnal rhythms except for nighttime locomotor activity, reduced from 3.7 +/- 0.4 to 2.8 +/- 0.3 counts/s. These data demonstrate that conscious rats respond to sustained orthostasis with hypertension, probably as a result of increased sympathetic output. Decreasing stress using a subanesthetic dose Flonase Tablets of chloralose increased this response, reducing the inhibitory effect on hypertensive responses.

minipress overdose 2017-06-25

Influence of postjunctional alpha 1- and subsequent alpha 2-adrenergic antagonism on myocardial blood flow was measured in a group of anesthetized cats with acute occlusion of the left anterior descending coronary artery (LAD) and a control group (n = 10 for both). The relatively selective postjunctional alpha 1-(doxazosin) and alpha 2-adrenergic (SK&F 104078) antagonists were applied after beta-adrenergic blockade (propranolol). Regional myocardial blood flow was obtained with radiolabeled microspheres. Major hemodynamic determinants for perfusion were kept constant both within and between groups by right atrial pacing and aortic obstruction. Mean coronary resistance in nonischemic myocardium was permanently lower in the occlusion group as compared with controls (p less than 0.01). Subsequent alpha 2-adrenergic antagonism reduced mean coronary resistance in controls only (p less than 0.05). Deltasone With Alcohol Cardiac output (CO) and dP/dt was reduced in LAD-occluded hearts after alpha 2-adrenergic blockade (p less than 0.01, p less than 0.05). The study demonstrates the significance of postjunctional alpha 2-adrenergic-mediated vasoconstriction in well-perfused myocardium of control hearts, whereas such vasoconstriction was deteriorated in LAD-occluded hearts. A role for myocardial alpha 2-adrenoceptors for maintenance of global cardiac function in acute regional ischemia was also indicated.

minipress overdose symptoms 2015-02-07

To evaluate the effect of Terazosin (alpha1 Vasaka Review adrenergic blocker) on bladder emptying in children with posterior urethral valves.

minipress medication information 2015-10-01

Previous studies have shown that a chemically reactive analog of prazosin, SZL-49, reduces the alpha-1 adrenoceptor population by a maximum of 60% (Kusiak et al., 1989). These data support the idea that alpha-1 receptor subtypes exist and only one is sensitive to alkylation by SZL-49. In the present study male rats were injected (i.p.) with SZL-49 (0.5-30 mg/ Coumadin 5 Mg kg) and the effects on [3H]prazosin binding, systemic arterial blood pressure and the pressor response to phenylephrine were assessed 24 hr later. SZL-49 treatment decreased the number of [3H]prazosin sites without affecting receptor affinity. The maximal reduction in binding sites was 60% (32 fmol/mg). At doses of 0.5-, 1-, 5- and 10-mg/kg SZL-49 reduced the receptor number to the same level (83 fmol/mg control; 47-60 fmol/mg treated). Injection of SZL-49 had no effect on resting blood pressure. However, drug treatment (0.5 mg/kg and greater) shifted the phenylephrine dose-response curve to the right. The maximal 1-, 5- and 10-mg/kg SZL-49, the ED50 for phenylephrine was approximately the same. Therefore, over a 20-fold range of SZL-49 concentrations no further reduction in receptor number or phenylephrine ED50 was observed. These data support the idea that S2L-49-sensitive and resistant alpha-1 receptors exist in vivo. The alkylation resistant receptor is capable of maintaining resting blood pressure. Furthermore, both receptors appear to be involved in mediating the increase in blood pressure observed with phenylephrine.

minipress and alcohol 2015-10-16

In rodents, extended access to cocaine produces an escalation in cocaine self-administration that has face and construct validity for human compulsive drug intake. Here we report that rats with six-hour access (long access, LgA) to Flomax Alternatives Generic cocaine self-administration produced a higher breakpoint for cocaine using a progressive-ratio schedule than rats with one-hour access (short access, ShA), and prazosin (alpha 1 receptor antagonist) reduced the higher breakpoint for cocaine in LgA rats. Additionally, the number of neurons with alpha 1-adrenergic receptor-like immunoreactivity in the bed nucleus of stria terminalis (BNST) was found to be much lower in LgA rats than in ShA and drug-naive rats. In contrast, UK14304 (alpha 2 receptor agonist) and betaxolol (beta 1 receptor antagonist) had no effect on cocaine self-administration in either group. The data suggest that activation of the alpha 1-noradrenergic system, perhaps in the BNST, is associated with increased motivation for cocaine in rats with extended access.

minipress medication 2017-06-04

We describe the clinical course and outcome in 46 victims of severe scorpion envenoming treated with prazosin (P), and compare them with earlier patients treated with conventional therapy (C) (n = 45) and nifepidine (N) (n = 28). The incidence of complicating left ventricular failure was 29% for C, 35% for N and 6.5% for P; that of acute pulmonary oedema was 46% for C, 14% for N and zero for Priligy 60 Mg P; mortality was 25% for C, 3.5% for N and zero for P. Although this is a historical study, prazosin appears to significantly reduce morbidity and shorten recovery time. Experience in other countries suggests that antivenom is helpful in controlling many of these problems, but in rural India serotherapy remains largely unavailable, and prazosin is a mainstay of treatment.

minipress dosage 2015-03-02

NA- and PE-induced contractile responses were attenuated proportionately with a decrease in extracellular pH (pHo), i.e. 7.4 → 6.8 → 6.0 → 5.5 → 5.0 → 4.5. Endothelium denudation increased the contractile response at both normal and acidic pHo. Prazosin (1 nM, 10 nM, and 0.1 μM) inhibited the Cymbalta Usual Dosage NA- and PE-induced contractile response at pHo 7.4 and the blocking effect of prazosin was potentiated at pHo of 6.0 and 5.0. RT-PCR analysis for α1D-AR in GSMA showed that the mRNA expression of α1D-AR was decreased under acidic pHo as compared to physiological pHo.

minipress cost 2017-11-17

Nitric oxide (NO) is one of the most important immune molecules in innate immunity of invertebrates, and it can be regulated by norepinephrine in ascidian haemocytes. In the present study, the mutual modulation and underlying mechanism between norepinephrine and NO were explored in haemocytes of the scallop Chlamys farreri. After lipopolysaccharide stimulation, NO production increased to a significant level at 24 h, and norepinephrine concentration rose to remarkable levels at 3 h and 12~48 h. A significant decrease of NO production was observed in the haemocytes concomitantly stimulated with lipopolysaccharide and α-adrenoceptor agonist, while a dramatic increase of NO production was observed in the haemocytes incubated with lipopolysaccharide and β-adrenoceptor agonist. Meanwhile, the concentration of cyclic adenosine monophosphate (cAMP) decreased significantly in the haemocytes treated by lipopolysaccharide and α/β-adrenoceptor agonist, while the content of Ca(2+) was elevated in those triggered by lipopolysaccharide and β-adrenoceptor agonist. When the haemocytes was incubated with NO donor, norepinephrine concentration was significantly enhanced during 1~24 h. Collectively, these results suggested that norepinephrine exerted varied effects on NO production at different immune stages via a novel α/β-adrenoceptor-cAMP/Ca(2+) regulatory pattern, and NO might have a feedback effect on the synthesis of norepinephrine in Zofran Reviews the scallop haemocytes.

minipress pill 2015-04-14

Quetiapine fumarate is an atypical antipsychotic with relatively benign side-effect profile. Here we report a rare side-effect of quetiapine use. This is the second reported case of peripheral edema with quetiapine use. Unaware of this rare side-effect, patient had to endure extensive investigations.

minipress 4 mg 2016-06-11

The concentration and location of adrenergic receptors in cat visual cortex have been determined by radioligand binding techniques using [3H]prazosin (alpha 1-adrenergic receptors), [3H]yohimbine (alpha 2-adrenergic receptors) and [3H]dihydroalprenolol (beta-adrenergic receptors). Saturable high affinity binding sites for all of these ligands were found. The beta-adrenergic receptor population was resolved into beta 1- and beta 2-sites that were present in the ratio 35:65. The laminar distributions of the alpha 1-, alpha 2- and beta-adrenergic receptors were different. The alpha 1- and beta-adrenergic receptors were very similarly localized, being seen in upper layers (I, II and III) and lower layers (layers V and VI). The labelling in upper layers was greater than that in lower layers, more so for alpha 1-adrenergic receptors than beta-adrenergic receptors. alpha 2-Adrenergic receptors were seen in a single band that occupied layer II and III but did extend to the pial surface. These results indicate that the effect of norepinephrine on neuronal activity in cat visual cortex will depend upon the layer in which it is released. Our results provide a basis for further physiological studies of the role of norepinephrine in the processing of visual information.

minipress drug class 2015-12-29

Chronic use of intranasal decongestants, such as oxymetazoline, leads to tachyphylaxis of response and rebound congestion, caused by alpha-adrenoceptor mediated down-regulation and desensitization of response.

minipress nightmares dosage 2017-02-03

5-Hydroxytryptamine (5-HT) induces rabbit detrusor contractions via 5-HT3 receptors. Similarly, 5-HT4 receptors are known to be present in the human bladder. Doxazosin, a non-selective alpha1 antagonist, is used for the symptomatic relief of bladder outflow obstruction. Previous work has shown that doxazosin inhibits 5-HT2-mediated platelet shape change. Hence, the aim of this study was to assess, using organ baths and autoradiography, whether doxazosin has any 5-HT-inhibiting activity in the rabbit detrusor. Detrusor strips from adult New Zealand White rabbits were placed in organ baths; phenoxybenzamine (10(-5) M) was added to block alpha-receptors. After KCl responses were assessed, the tissues were exposed to 10(-3) M 5-HT. Subsequently, the strips were incubated with doxazosin or ondansetron (10(-5) M; 5-HT3 antagonist) followed by a further exposure to 5-HT. In some experiments, after the initial 5-HT-induced contractions, the tissues were washed and then re-exposed to 5-HT. These latter experiments acted as controls. Low-resolution autoradiography was performed on detrusor sections to assess the effect of doxazosin on 5-HT binding. These sections were analyzed densitometrically. Doxazosin and ondansetron produced a significant reduction in 5-HT-mediated contractions. Inhibition by doxazosin was in a concentration-dependent manner. Autoradiography demonstrated a significant reduction in [3H]-5-HT binding by doxazosin. Doxazosin significantly inhibits 5-HT-mediated contractions in the rabbit detrusor. This effect appears to be mainly mediated via 5-HT3 receptor inhibition. Autoradiographic evidence suggests that doxazosin reduces 5-HT binding in the rabbit detrusor. The beneficial effects of doxazosin in bladder outflow obstruction may be due, at least in part, to 5-HT antagonism.

minipress ptsd dosage 2015-08-31

Experiments were done in isolated, perfused mesenteric vascular beds from Sprague-Dawley rats. Bolus injections of norepinephrine (3-100 nmol) induced dose-dependent increases in perfusion pressure with a maximum increase greater than 100 mm Hg. In the same dose range, clonidine had no effect on perfusion pressure. In the presence of an elevated pressure caused by constant infusions of norepinephrine (6-20 microM), bolus injections of clonidine (0.1-10 nmol) or acetylcholine (0.007-7 nmol) caused dose-related decreases in perfusion pressure. Procedures which damage endothelium (brief exposure to methylene blue or reactive oxygen radicals) abolished the depressor action of acetylcholine but only moderately reduced the depressor action of clonidine. The depressor action of clonidine was not antagonized by the alpha-2 adrenoceptor antagonist, idazoxan. Acetylcholine produced depressor responses in the presence of 5-hydroxy-tryptamine or vasopressin, but clonidine did not. Dose-response curves to bolus doses of norepinephrine were shifted markedly to the right by an alpha-1 selective concentration of prazosin (1 nM) and were shifted to the right with depression of maximum by infusions of clonidine (0.3 and 1.0 microM). It is concluded that, in the mesenteric vasculature of the rat: 1) the role of alpha-2 adrenoceptors, in responses to clonidine, is minimal; 2) endothelial factors play little role, if any, in the depressor effects of clonidine and 3) clonidine has a potent ability to interfere with the alpha-1 adrenoceptor-mediated vasoconstriction induced by norepinephrine. This antagonistic action may be at the level of the receptor but could involve postreceptor steps.

minipress max dose 2015-09-11

α1-adrenoceptor density and the affinity of CUMI-101 for these receptors were similar across species. Cerebellar binding potentials were 3.7 for humans, 2.3 for monkeys, and 3.4 for rats.