Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nineteen patients with essential hypertension (EH) were studied as outpatients. After administration of chlorthalidone, 50 mg/day for 4 weeks, prazosin 1-4 mg/day (1.82 +/- 0.33 mg/day) was added for a period of 12 weeks. Prazosin lowered supine blood pressure from 149.7 +/- 2.85/102.0 +/- 2.75 mm Hg to 128.2 +/- 3.0/86.1 +/- 1.04 mm Hg (p less than 0.001). Prazosin did not alter heart rate significantly. Prazosin increased the thyroid stimulating hormone (TSH) from 3.63 +/- 0.33 microunits/ml to 4.83 +/- 0.45 microunits/ml (p less than 0.025), thyroxine (T4) from 10.03 +/- 0.29 micrograms/ml to 10.85 +/- 0.42 micrograms/ml (p less than 0.005), and decreased triiodothyronine (T3) from 36.65 +/- 0.62% to 35.42 +/- 0.56%, which was not significant. The free thyroxine index (FTI) increased slightly from 3.67 +/- 0.12 to 3.83 +/- 0.14 (p less than 0.025). However, all values remained within the normal range for the laboratory. Serum cholesterol increased insignificantly. Triglycerides decreased significantly from 223.4 +/- 50.6 mg/dl to 161.7 +/- 29.0 mg/dl (p less than 0.05). High density lipoproteins (HDL) increased significantly from 30.1 +/- 2.1% to 36.0 +/- 3.06 (p less than 0.025). Low density lipoproteins (LDL) decreased insignificantly and very low density lipoproteins (VLDL) decreased from 20.9 +/- 3.44 to 16.3 +/- 2.85 (p less than 0.005). The cholesterol ratio increased from 45.51 +/- 4.3 to 64.71 +/- 10.7 (+42.1%). These results indicate that, in patients with essential hypertension, prazosin is an effective antihypertensive agent and that it significantly increases HDL, decreases VLDL, and improves the cholesterol ratio.
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PMID:Effect of prazosin on blood lipids and on thyroid function in hypertensive patients. 617 61

The effects of propranolol and prazosin on plasma lipoproteins in patients with essential hypertension were evaluated according to a crossover protocol of two 8-week periods with a washout of 4 to 6 weeks. Eleven patients with moderate hypertension (greater than 90 but less than or equal to 144 mm Hg, diastolic) and slightly overweight (+10% to +/- +30%, according to Metropolitan Life Insurance tables) were selected. No dietary changes were prescribed. Plasma cholesterol, triglycerides (TG), and lipoprotein changes were monitored at the beginning of each sequence and at 2-, 4- and 8-week intervals. Prazosin, when given first, did not essentially modify any of the metabolic parameters, except for a slight elevation in plasma apoprotein AI levels, i.e., the main protein component of high density lipoprotein (HDL); propranolol caused a significant rise in total TG and very low density lipoprotein TG (VLDL-TG) levels (+37.3% and +23.9%, respectively). Somewhat lower total TG (+19.6%) and vLDL (17.8%) TG elevations were noted when propranolol was given first; plasma glucose was also significantly raised (+12.8%). Triglyceride and glucose levels returned to normal upon changing to prazosin. Total plasma- and lipoprotein-associated cholesterol levels were essentially unchanged with either drug; similarly, no significant changes were detected in total plasma apoprotein B (the main protein component of LDL and also VLDL), a component of apoprotein AI levels. Uric acid levels were slightly raised on propranolol. There was an 8.8% reduction in uric acid levels when the medication changed from propranolol to prazosin.
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PMID:Plasma lipid and lipoprotein changes in hypertensive patients treated with propranolol and prazosin. 617 63

We studied peripheral and central hemodynamics and plasma catecholamine levels in 12 previously untreated patients with essential hypertension before and during treatment with the alpha 1-adrenoceptor antagonist prazosin (9.8 +/- 1.1 mg/day for 3-6 weeks following dose titration) as a single drug. Prazosin did not alter intra-arterially recorded blood pressures in the group as a whole, in spite of adequate plasma levels (12.6 +/- 1.2 ng/ml). There were no changes in cardiac output, blood volume, systemic or forearm vascular resistance, or forearm venous tone at rest during treatment. The blood pressure response to prazosin was correlated to pretreatment systemic and forearm vascular resistances. Arterial adrenaline levels were unchanged, but noradrenaline levels increased from 1.30 +/- 0.10 to 1.85 +/- 0.20 nM (p less than 0.05). Both noradrenaline and blood pressure responses to isometric hand-grip exercise were delayed and reduced during treatment. The hemodynamic and plasma catecholamine responses to a cold pressor test and tilting (50% head-up during 10 min) were similar before and during treatment. Our results may be related to development of tolerance to the alpha-adrenoceptor blocking effect of prazosin during long-term treatment. The elevation of arterial noradrenaline levels suggests that increased sympathetic activity also may have opposed the hypotensive response to prazosin.
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PMID:Effects of prazosin on hemodynamics and sympatho-adrenal activity in hypertensive patients. 619 Nov 36

Patients with essential hypertension (n = 45) had significantly lower substance P plasma levels (13.6 +/- 2.30 pg/ml) in comparison with a group of 24 normotensive subjects (45.4 +/- 7.18 pg/ml) analyzed by radioimmunoassay. Prazosin treatment for 2 weeks with 4.5 mg/day enhanced the substance P plasma level depending on its antihypertensive effect. Norepinephrine concentration in plasma was also elevated by prazosin. Dipeptidylpeptidase IV, dopamine-beta-hydroxylase and plasma renin activity were not changed significantly. The results indicate the participation of substance P in pathophysiological processes of human essential hypertension.
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PMID:Evidence of decreased plasma substance P levels in human essential hypertension and influence of prazosin treatment. 619 65

Prazosin, a peripherally active alpha-adrenoceptor antagonist, and clonidine, a centrally active alpha-adrenoceptor agonist, both reduce blood pressure but with different alterations in sympathetic nervous system activity. We studied the effects of monotherapy with either prazosin or clonidine in 10 and 30 patients, respectively, with essential hypertension. Prazosin reduced blood pressure without affecting heart rate or circulating plasma catecholamines. Sensitivity to injected phenylephrine was markedly reduced by prazosin, and sensitivity to isoproterenol was increased, whereas baroreflex sensitivity was not significantly altered. Blood pressure response to prazosin was correlated with basal plasma norepinephrine concentration (r = 0.64, P less than 0.04). In contrast, clonidine reduced heart rates and plasma concentrations of both norepinephrine and epinephrine, increased the sensitivity to phenylephrine, and increased baroreflex sensitivity. Blood pressure response to clonidine was correlated with reduction in plasma norepinephrine concentration (r = 0.51, P less than 0.004). Thus, blood pressure reduction resulting from monotherapy with either prazosin or clonidine occurs through different antisympathetic effects, suggesting that combined therapy might be useful in those unresponsive to either drug alone.
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PMID:Effects of prazosin and clonidine on sympathetic and baroreflex function in patients with essential hypertension. 663 May 84

Abnormal sympathetic function has been proposed as a factor in the development of essential hypertension. If this is the case, prazosin hydrochloride, which works by a selective, peripheral, antisympathetic effect--postsynaptic alpha blockade--may have an advantage over other antihypertensive agents. In this study, blood pressure response and measures of sympathetic and baroreflex function were followed in 13 hypertensive patients. Prazosin alone significantly reduced standing and sitting diastolic blood pressures without affecting pulse rates, plasma catecholamines or baroreflex slopes in all patients. The addition of a thiazide diuretic in persons who did not achieve goal blood pressure on prazosin alone was generally successful in reducing blood pressure to desired levels, and increased both plasma renin activity and aldosterone concentrations. No significant relation was apparent between specific characteristics of sympathetic function and response to prazosin as initial therapy, although patients responding tended to have initially higher plasma norepinephrine concentrations.
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PMID:Prazosin as initial antihypertensive therapy: correlates of sympathetic function. 669 63

The effects of prazosin and propranolol on total serum cholesterol concentration, low-density lipoprotein and high-density lipoprotein cholesterol fractions, and serum triglyceride concentration were compared in a crossover study in 29 patients with mild to moderate essential hypertension. All patients received polythiazide at a constant dose throughout control and drug treatment periods. Comparable blood pressure reduction was achieved with prazosin (9.3 +/- 7.1 mg per day) and propranolol (183.6 +/- 154.5 mg per day). Prazosin administration was associated with a significant reduction in the concentrations of total serum cholesterol (-5.5 percent), triglyceride (-20.0 percent), and low-density lipoprotein cholesterol (-10.1 percent). High-density lipoprotein cholesterol concentration increased (+8.0 percent) as did the ratio high-density lipoprotein: total cholesterol (+14.1 percent). No significant changes in any of the serum lipid fractions were observed during propranolol administration.
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PMID:Effects of prazosin and propranolol on serum lipids in patients with essential hypertension. 670 64

Prazosin was administered to 16 patients with essential hypertension in an initial dose of 0.5 mg, after which the blood pressure (BP), pulse, and plasma concentrations of prazosin were measured at 0, 0.5, 1, 1.5, 2, 2.5, 3, 4, 6, 8, and 24 hours. The dose of prazosin was then increased over 16 to 20 weeks, and similar sequences of measurements were obtained twice. Eleven patients completed the 20-week course. All patients did not respond in a similar way; two distinct patterns of BP and pulse response emerged, although there was no significant difference in the pharmacokinetic parameters, namely, absorption rate constant (Ka), maximum plasma concentration (Cpmax), time to reach the maximum concentration (Tmax), prazosin plasma half-life (T 1/2), elimination rate constant (kel), prazosin plasma concentration-time curve (AUC), and clearance. Patients in Group 1 had a marked reduction (52/30 mm Hg) of BP after the first dose of prazosin, no pulse increase, and needed a small dose of prazosin to maintain an adequate BP response. Patients in Group 3 had a minimal reduction in BP (14/13 mm Hg) after a first dose, a significant pulse increase, and needed a high dose of prazosin to control their BP. We conclude that this effect might be due to a different drug-receptor interaction, and the BP response and dose could be predicted from the response of the first dose of prazosin.
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PMID:Prazosin plasma concentration and blood pressure reduction. 706 Nov 32

Prazosin, an antihypertensive agent that reduces blood pressure (BP) mainly through a blockade of alpha-adrenergic receptors, may, in theory, affect sympathetic control of circulation to an extent that impairs circulatory hemeostasis. This possibility was studied in subjects with essential hypertension by examining the cardiovascular effects of several stimuli that induce a powerful and diversified activation of the sympathetic noradrenergic activity (dynamic and isometric exercise, cold exposure) and of stimuli that exert a powerful inhibitory influence upon the sympathetic nervous system (carotid baroreceptor reflex). Before and after 15 days of continuous administration of prazosin (2-5 mg), 3 times a day, measurements were made of BP (intraarterial catheter), heart rate, cardiac output (thermodilution), and peripheral resistance. Prazosin reduced mean arterial pressure (10%) and peripheral resistance (9%) at rest, and it did not affect heart rate and cardiac output. Neurally mediated changes in arterial pressure, cardiac output, and peripheral resistance during dynamic or isometric exercise and cold exposure were unaffected by the drug; also unaffected were the cardiovascular responses to increase and decrease in carotid baroreceptor activity obtained by varying carotid transmural pressure through a variable neck pressure chamber device. Thus, the hypotensive and vasodilating effect of prazosin in essential hypertension is not accompanied by an impaired response to neural excitation influences upon the cardiovascular system. Also, the inhibitory influences originating from the carotid baroreflex are unchanged. These data indicate that circulatory homeostasis is largely preserved during administration of prazosin at clinically effective doses.
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PMID:Effects of prazosin on autonomic control of circulation in essential hypertension. 741 71

Secretion of insulin, glucagon, gastrin and pancreatic polypeptide (PP) at basal and test meal stimulation conditions were investigated in 17 patients with essential hypertension (EH) before and after 12 months of treatment with prazosin and in 10 healthy subjects. Before prazosin therapy, patients with EH differ from healthy subject higher insulin and gastrin but lower PP secretion after test meal stimulation. 12 month therapy with prazosin enhanced insulin and suppressed gastrin secretion stimulated by test meal in comparison to the pretreatment values. Prazosin therapy did not influence significantly glucagon and PP secretion. Our results suggest, that long term prazosin treatment markedly influenced insulin and gastrin secretion in patients with EH.
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PMID:[Effect of long term prazosin treatment on secretion of insulin, glucagon, gastrin, and pancreatic polypeptide in patients with essential hypertension]. 847 41


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