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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of jingsongling (JSL) and xylazine on heart rate (HR) and mean arterial pressure (MAP) were studied in five conscious male dogs. An i.v. injection of xylazine (1 mg/kg) caused a bradycardia, an initial hypertension, and a subsequent hypotension. An i.v. injection of JSL (1 mg/kg) caused a bradycardia and a 20-min hypertension without a subsequent hypotension. Atropine sulfate (45 micrograms/kg, i.v.) increased HR for 30 min without changing MAP, and antagonized JSL-induced bradycardia for at least 60 min. There was a subsequent rebound bradycardia. Atropine sulfate potentiated JSL-induced hypertension in both magnitude and duration. Yohimbine (0.1 mg/kg, i.v.), an alpha 2-adrenoceptor antagonist, increased HR and MAP for 110 and 70 min, respectively. Yohimbine not only failed to potentiate but even reversed the pressor effect of JSL in a dose-dependent manner. Yohimbine also caused a dose-dependent reversal of JSL-induced bradycardia. Tolazoline (5 mg/kg, i.v.), a nonselective alpha-adrenoceptor antagonist, increased MAP for 20 min without changing HR. Tolazoline also reversed JSL-induced hypertension and bradycardia. Prazosin (1 mg/kg), an alpha 1-adrenoceptor antagonist, decreased MAP and increased HR for at least 110 min. Prazosin reversed JSL-induced hypertension but failed to affect JSL-induced bradycardia. These results indicated that: (1) JSL-induced bradycardia and hypertension are mediated by alpha 2-adrenoceptors; (2) yohimbine and tolazoline may be useful in antagonizing these untoward reactions associated with JSL administration, whereas prazosin and atropine were not found to be beneficial in this regard.
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PMID:The effects of jingsongling, a xylazine analog, on mean arterial blood pressure and heart rate in dogs--influences of yohimbine, tolazoline, prazosin, and atropine. 281 Apr 77

The relationship between alpha-adrenoceptor number and response has been studied in rabbits under a range of physiological and pathological conditions. The effects of irreversible alpha-adrenoceptor blockade, maturation, ageing, oestrogen treatment, adrenaline infusion, perinephritis hypertension and sinoaortic denervation on alpha-adrenoceptor number and response were examined. alpha-Adrenoceptor number was measured by radioligand binding. [3H]Prazosin and [3H]clonidine were used as ligands to measure alpha 1- and alpha 2-adrenoceptor number in spleen and [3H]yohimbine to measure alpha 2-adrenoceptor number on platelets. Responses in vivo were studied by examining the pressor responses to a range of alpha-adrenoceptor agonists. The functional response of platelets was examined in vitro by using the aggregatory response to adrenaline. Reductions in alpha 2-adrenoceptor ligand binding were consistently accompanied by equivalent reductions in alpha 2-adrenoceptor-mediated responses. In contrast large reductions in [3H]prazosin binding were observed with little or no change in alpha 1-adrenoceptor-mediated responses. These results would be consistent with a large receptor reserve for alpha 1-adrenoceptors but few if any spare alpha 2-adrenoceptors in the vasculature or on platelets. Increased responses to both alpha 1- and alpha 2-adrenoceptor agonists were observed in animals with sinoaortic denervation and to alpha 1-adrenoceptor agonists in rabbits with perinephritis hypertension. These increases in response were not accompanied by increases in radioligand binding and may be related to alterations in the coupling of receptor activation to end-organ response.
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PMID:alpha-Adrenoceptor regulation in vivo and in vitro in the rabbit. 285 7

The hypotensive effect of vasodilator monotherapy in hypertension is attenuated by a baroreceptor-mediated increase in the sympathetic release of noradrenaline. Nifedipine induces a rise in noradrenaline release, but it is not known to affect noradrenaline-induced vascular contraction of smooth muscle to a clinically significant degree. The haemodynamic and hormonal effects of a single sublingual dose of nifedipine 20 mg in 8 moderately hypertensive patients have been studied before and during postsynaptic alpha 1-blockade with prazosin. The antihypertensive effect of nifedipine was significantly increased by prazosin pretreatment (fall in mean arterial pressure 60 min after nifedipine: -16.7% with and -8.5% without prazosin), despite similar increases in plasma noradrenaline. Prazosin alone caused no change in supine blood pressure for 2 h after an oral dose of 2 mg. The findings are in keeping with the hypothesis that prazosin blocks a compensatory reaction to vasodilatation caused by nifedipine.
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PMID:The influence of alpha 1-adrenergic blockade on the acute antihypertensive effect of nifedipine. 286 64

Prazosin is a quinazoline derivative, which lowers blood pressure by selective alpha-1-receptor antagonism. It has been found that, for similar decreases in blood pressure, prazosin causes less reflex tachycardia than non-selective alpha blockers or direct vasodilators, and that it is as efficacious as other conventional antihypertensive agents (alpha-methyldopa, hydralazine, beta blockers, etc.) in controlling severe hypertension. Prazosin causes a dose-related decrease in blood pressure in humans; twice-daily dosing is sufficient for 24-hour blood pressure control. Prazosin in combination with other drugs has also been shown to control blood pressure effectively, and it has been associated with relatively few side effects. Other agents with selective alpha-1-receptor-blocking activity are under investigation: these include doxazosin, trimazosin, terazosin, and alfuzosin.
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PMID:Clinical pharmacology and therapeutic role of prazosin and related alpha-adrenoceptor antagonists. 287 58

This review examines the effects of various antihypertensive drugs on blood lipids, lipoproteins, and apolipoproteins. A large number of studies have documented the elevation of total cholesterol, triglycerides, low density lipoprotein (LDL) cholesterol, and very-low density lipoprotein (VLDL) cholesterol with many thiazide-type diuretic drugs, albeit mainly in short term studies. When added to thiazide diuretics, both beta 1-selective and non-selective beta-blocking drugs elevate total triglycerides and VLDL triglycerides, lower high density lipoprotein (HDL) cholesterol and raise the ratio of total cholesterol to HDL cholesterol ratio. Most non-selective beta-blockers have similar effects when used as monotherapy, but the beta 1-selective agents appear not to affect HDL cholesterol in monotherapy. Prazosin appears free of adverse lipid effects and has improved lipid-lipoprotein concentrations in many studies. Preliminary data on several other drugs also suggest a favourable lipid profile and additional study is warranted - among these are guanabenz, clonidine, pindolol, labetalol, indapamide, and guanfacine. Elevations in serum triglycerides are often ignored on various counts, but triglycerides have been found to be a strong risk factor in European studies and in women over the age of 50 years in the Framingham study. Despite the unfavourable short term effects of diuretics, the theoretical risk of the lipid-lipoprotein changes remains unclear because HDL cholesterol and the total cholesterol to HDL cholesterol ratio are often unchanged. For this and other reasons, a long term trial comparing thiazide-type diuretics with drugs with the most favourable lipid-lipoprotein profile is needed. Until this is accomplished, in most settings diuretic-based regimens are still preferred initially since they are of proven, if limited, efficacy against the cardiovascular complications of hypertension.
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PMID:The effects of antihypertensive drugs on serum lipids and lipoproteins. II. Non-diuretic drugs. 287 46

Chronic (3-day) treatment with prazosin causes an increase in renal alpha 2-adrenergic receptor density and the relocation of renal tubular alpha 2-adrenergic receptors from extrajunctional to postjunctional sites. We investigated whether chronic prazosin treatment (2 mg/kg, i.p.) caused a functional alteration of other renal alpha 2-adrenergic receptors, using the isolated perfused rat kidney. Prazosin significantly reduced blood pressure and increased heart rate during the 3-day treatment. Renal nerve stimulation (2-8 Hz, 10 V, 1 msec) caused a frequency-dependent increase in renovascular resistance, which was potently blocked by prazosin in vitro in both control and prazosin-treated rat kidneys. The vasoconstrictor response to the alpha 2-adrenergic receptor-selective agonist BHT 933 (3-300 microM) was significantly higher in kidneys from prazosin-treated rats. Yohimbine (3-300 nM) potentiated the response to renal nerve stimulation in both treatment groups. The increase in vascular resistance following renal nerve stimulation was lower in kidneys from prazosin-treated rats, but the response to the alpha 1-adrenergic receptor agonist methoxamine (0.3-1 microM) was unchanged. Further studies revealed that renal nerve stimulation-evoked norepinephrine release from prazosin-treated rat kidneys was significantly lower than release from untreated controls. This response could be normalized to control levels by a combination of cocaine (10 microM) and yohimbine (100 nM). Thus, chronic prazosin treatment caused enhanced alpha 2-adrenergic receptor-mediated vasoconstriction and facilitated renal prejunctional inhibitory mechanisms. We conclude that with chronic alpha 1 adrenergic receptor blockade there is increased alpha 2-adrenergic receptor function in at least two and possibly three sites in the kidney; these include postjunctional tubular, prejunctional vascular, and possibly extra-junctional vascular sites.
Hypertension 1987 Jun
PMID:Prazosin-induced alterations in renal alpha-adrenergic receptor function. 288 71

Hypertension and diabetes mellitus frequently coexist and are independent risk factors for reduced peripheral perfusion. Antihypertensive medications that reduce blood pressure and improve peripheral perfusion would have advantages in diabetic hypertensive patients. In a randomized, two-placebo-period, single-blind, two-way, crossover study, finger and forearm blood flow, lipid levels, and blood pressure control were determined in 19 diabetic hypertensive patients given prazosin and atenolol, with each drug and placebo period lasting four weeks. Both drugs reduced blood pressure (sitting, 157/95 to 142/84 mm Hg for atenolol and 155/95 to 138/82 mm Hg for prazosin; standing, 154/94 to 144/84 mm Hg for atenolol and 154/94 to 133/81 mm Hg for prazosin). Lipid levels did not change, except that low-density lipoprotein levels decreased from 148 to 127 mg/dl with prazosin. Atenolol did not change forearm or finger blood flow or vascular resistance. Prazosin increased blood flow and reduced vascular resistance in both finger and forearm. In conclusion, prazosin demonstrated a potentially more appropriate hemodynamic profile than atenolol in diabetic hypertensive patients in this study.
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PMID:Forearm and finger hemodynamics, blood pressure control, and lipid changes in diabetic hypertensive patients treated with atenolol and prazosin. A brief report. 291 73

Long-term treatment of hypertensive rats with arterial vasodilators may further increase left ventricular hypertrophy. Since left ventricular hypertrophy may be an important determinant of outcome in hypertension, the long-term effects of arterial vasodilation with hydralazine on left ventricular mass and function were compared with those of an alternative third-line drug, the alpha1 blocker prazosin, in patients still hypertensive despite combined diuretic and beta blocker therapy. A single-blind, randomized, two-group parallel design was employed. Both treatments induced a sustained antihypertensive effect, with hydralazine showing more effect on supine blood pressure, and prazosin having more effect on standing pressure. Heart rate, cardiac output, and volume status showed only minor changes. Plasma norepinephrine showed a sustained increase when measured in both the supine and standing positions, but the increases were similar for the two treatments. Supine and standing plasma renin activity increased only during long-term treatment with hydralazine. Prazosin induced a progressive decrease in left ventricular mass over time (-34 +/- 15 g/m2 at 12 months), but hydralazine did not (-9 +/- 10 g/m2 after 12 months). Stepwise regression indicated that a decrease in systolic blood pressure was associated with a decrease in left ventricular mass with both treatments, but an increase in plasma norepinephrine was associated with an increase in left ventricular mass only with hydralazine, suggesting that increased sympathetic activity may affect left ventricular mass via cardiac alpha1 receptors. Thus, if regression of left ventricular hypertrophy is a worthwhile therapeutic goal, hydralazine and analogous arterial vasodilators are not drugs of choice.
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PMID:Vasodilators and regression of left ventricular hypertrophy. Hydralazine versus prazosin in hypertensive humans. 295 39

The effect of amitraz on heart rate (HR) and mean aortic blood pressure (MAP) were studied in five conscious male dogs. An iv injection of amitraz (1 mg/kg) caused a decrease in HR, which was accompanied by sinus arrhythmia for at least 60 min. Administration of amitraz also caused an increase in MAP for 20 min. Atropine sulfate (0.045 mg/kg, iv) increased HR and prevented amitraz-induced bradycardia. In addition, atropine potentiated amitraz-induced hypertension for 45 min. Yohimbine, an alpha 2-adrenoreceptor antagonist, given iv at 0.1 mg/kg, prevented hypertension, bradycardia, and sinus arrhythmia induced by amitraz. Tolazoline, a nonselective alpha-adrenoreceptor antagonist, given iv at 5 mg/kg, reduced the bradycardia and sinus arrhythmia caused by amitraz administration but did not change amitraz-induced hypertension. Tolazoline alone also increased both HR and MAP. Prazosin, an alpha 1-adrenoreceptor antagonist, given iv at 1 mg/kg, did not affect the cardiovascular actions of amitraz. The results suggest that (1) alpha 2-adrenoreceptors mediate amitraz-induced bradycardia and hypertension, and (2) yohimbine, but not atropine, can be used to control the untoward reactions of amitraz.
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PMID:Effect of amitraz on heart rate and aortic blood pressure in conscious dogs: influence of atropine, prazosin, tolazoline, and yohimbine. 301 23

Hypertension and diabetes mellitus frequently coexist and are independent risk factors for reduced peripheral perfusion. Antihypertensive medications that reduce blood pressure and improve peripheral perfusion would have advantages in diabetic patients with hypertension. In a randomized, two-placebo period, single-blind, two-way crossover study, we determined finger and forearm blood flow, lipid levels, and blood pressure control in 19 diabetic patients with hypertension, with each atenolol or prazosin and placebo period of 4 weeks' duration. Both drugs reduced blood pressure (sitting: 157/95 to 142/84 mm Hg, atenolol; 155/95 to 138/82 mm Hg, prazosin; standing: 154/94 to 144/84 mm Hg, atenolol; 154/94 to 133/81 mm Hg, prazosin). Lipid levels did not change except that low-density lipoprotein levels fell from 148 to 127 mg/dl with prazosin. Atenolol did not change forearm or finger blood flow or vascular resistance. Prazosin increased blood flow and reduced vascular resistance in both finger and forearm. In conclusion, prazosin has a potentially more appropriate hemodynamic profile than has atenolol in diabetic patients with hypertension.
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PMID:Forearm and finger hemodynamics, blood pressure control, and lipid changes in patients with diabetic hypertension treated with atenolol and prazosin. 329 75


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