Gene/Protein Disease Symptom Drug Enzyme Compound
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 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fifty-one patients with essential hypertension, 22 males and 29 females with a mean age of 51 (range, 28 to 65 years), were studied for more than 12 months in a controlled clinical trial with nitrendipine, a new calcium antagonist agent. No differences in age, severity of hypertension, and other risk factors between the two sexes were detected. Forty-four of 51 patients completed the study, and 38 (86.4%) achieved a normalization of blood pressure. Mean systolic blood pressure decreased from 196.0 +/- 12.9 mm Hg (means +/- SD) during placebo to 171.2 +/- 9.5 mm Hg (12.6%, p less than 0.001) after 12 months. Mean diastolic blood pressure at the same time decreased from 109.0 +/- 5.2 mm Hg to 88.5 +/- 3.6 mm Hg (18.8%, p less than 0.001). Heart rate also decreased slightly but significantly (p less than 0.01) after the fifth week. A significant change in weight was not observed throughout the trial. Plasma potassium remained unchanged during the year, and plasma sodium after a transient increase (p less than 0.001) in the fifth week returned very close to basal levels in the sixth month. Side-effects were observed in 17 patients, 5 of whom had to leave the trial, but in the rest they were usually mild and transient. These were mainly frontal and occipital headache, facial flushing, ankle and pretibial oedema, and dizziness. No relationship was detected between side-effects and body weight or plasma sodium disturbances. Preliminary data on a separate group of 27 elderly patients (66-83 years) showed a better and faster effect of nitrendipine given in low doses.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical experience with long-term nitrendipine treatment in essential hypertension. 608 73

To determine whether E-643, a new alpha-blocking agent, would reduce the blood pressure, regardless of the posture, a 1 mg dose was given 3 times daily for 7 consecutive days, to 8 male and 7 female inpatients, aged 37--73 years, with essential hypertension. Blood pressure and pulse rate were measured daily in the supine, sitting and standing positions. Before and after the treatment with E-643, plasma levels of noradrenaline, adrenaline, dopamine-beta-hydroxylase, renin and aldosterone were determined, samples being obtained with the subjects recumbent and after standing upright for 60 min. A significant reduction in the systolic and diastolic blood pressures was evident in the supine (172 +/- 31/100 +/- 12 leads to 151 +/- 28/89 +/- 14 mmHg), sitting (158 +/- 22/101 +/- 11 leads to 138 +/- 28/89 +/- 15 mmHg) and standing (153 +/- 32/103 +/- 21 leads to 129 +/- 31/89 +/- 20 mmHg) positions. The reduction in blood pressure remained unchanged throughout the period of administration of E-643. Pulse rate was not affected when the subjects were supine (67 +/- 10 leads to 69 +/- 10 beats/min), but was increased in the sitting (68 +/- 10 leads to 73 +/- 9 beats/min) and standing (73 +/- 10 leads to 81 +/- 11 beats/min) positions. The increased pulse rate tended to decline during continued administration of E-643. Treatment with E-643 produced no significant change in plasma levels of adrenaline, noradrenaline, dopamine-beta-hydroxylase, renin and aldosterone. The antihypertensive effect of treatment was more prominent in the patients with higher levels of plasma catecholamines and dopamine-beta-hydroxylase, and was less prominent in those with higher plasma renin and aldosterone. Two patients had temporary bouts of dizziness and visual disturbances, but there were no subjective complaints during treatment.
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PMID:Antihypertensive effect of E-643, a new alpha-adrenergic blocking agent. 611 9

Prizidilol is a new antihypertensive agent reported to possess combined precapillary vasodilator and betareceptor-blocking properties. To clarify the profile of the acute effects of prizidilol in man, a variable dose study was performed in 8 patients with benign essential hypertension. Blood pressure, heart rate, plasma renin activity, aldosterone, plasma and urinary catecholamines and electrolytes were determined at short intervals before and up to 23 h after oral administration of placebo and prizidilol 150, 300 and 600 mg. The 4 studies were performed at weekly intervals according to a Latin square design. Prizidilol produced dose-dependent decreases in supine and upright blood pressure, with an initial change after about 2 h and maximal effects from 4 to 8 h after drug ingestion. Following a high dose of prizidilol, supine mean blood pressure (average 128 mmHg prior to treatment) was normalised (less than 107 mmHg) from 3 to 7 h and was still below predose level 23 h after ingestion. The only reported side effects were postural dizziness in 2 cases (corresponding to a fall in systolic upright blood pressure to less than 95 mmHg) and headache in one case. A biphasic variation in heart rate and plasma renin activity, with an early drop and a subsequent tendency to a slight rise, was observed after an intermediate or high dose of prizidilol. Plasma norepinephrine levels were increased by a high dose of prizidilol, while plasma epinephrine, aldosterone and plasma and urinary electrolytes were not consistently changed. Prizidilol in a a single oral dose appeared to be a potent antihypertensive agent. The profile of heart rate and plasma renin point to early dominance of beta-blockade followed by appearance of the concomitant vasodilator properties of prizidiol.
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PMID:Acute effects of prizidilol on blood pressure, heart rate, catecholamines, renin and aldosterone in essential hypertension. 612 41

17 subjects with essential hypertension (14 male, 3 female - ages: 40-69 years), 13 of whom continued their previous anti-hypertensive therapy, completed a double-blind cross-over trial of ketanserin 40 mg twice daily versus placebo tablets twice daily - each treatment phase was six weeks in duration. For the group as a whole, blood pressure (BP) was reduced in the ketanserin phase compared with the placebo phase; supine mean BP decrease: 4 +/- 1 mm Hg (p less than 0.05); standing mean BP decrease: 7 +/- 1 mm Hg (p less than 0.001). Heart rate (HR) was also significantly decreased in the ketanserin phase by 5 +/- 1 beats/minute (p less than 0.001). When individual subgroups were analysed the reductions in BP and HR were greater in subjects already receiving anti-hypertensives, diuretic and/or beta blockers. Changes were observed in 24 hour urine sodium and potassium excretion - sodium (mmol/day): placebo 137 +/- 17, ketanserin 174 +/- 19 (p less than 0.05); potassium (mmol/day): placebo 74 +/- 8, ketanserin 57 +/- 5. For the group as a whole there were no significant adverse effects during the ketanserin phase, although two subjects had a dose reduction of ketanserin because of drowsiness and dizziness. Two additional subjects withdrew from the study due to adverse effects, one in the placebo phase. In conclusion ketanserin in the dose administered has a modest hypotensive effect which is best seen in subjects already receiving other anti-hypertensive agents.
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PMID:The effect of ketanserin on blood pressure and biochemical parameters in treated patients with essential hypertension. 614 14

Labetalol is a combined alpha- and beta-adrenoceptor blocking agent for oral and intravenous use in the treatment of hypertension. It is a nonselective antagonist at beta-adrenoceptors and a competitive antagonist of postsynaptic alpha 1-adrenoceptors. Labetalol is more potent at beta that at alpha 1 adrenoceptors in man; the ratio of beta-alpha antagonism is 3:1 after oral and 6.9:1 after intravenous administration. Labetalol is readily absorbed in man after oral administration, but the drug, which is lipid soluble, undergoes considerable hepatic first-pass metabolism and has an absolute bioavailability of approximately 25%. There are no active metabolites, and the elimination half-life of the drug is approximately 6 hours. Unlike conventional beta-adrenoceptor blocking drugs without intrinsic sympathomimetic activity, labetalol, when given acutely, produces a decrease in peripheral vascular resistance and blood pressure with little alteration in heart rate or cardiac output. However, like conventional beta-blockers, labetalol may influence the renin-angiotensin-aldosterone system and respiratory function. Clinical studies have shown that the antihypertensive efficacy of labetalol is superior to placebo and to diuretic therapy and is at least comparable to that of conventional beta-blockers, methyldopa, clonidine and various adrenergic neuronal blockers. Labetalol administered alone or with a diuretic is often effective when other antihypertensive regimens have failed. Studies have shown that labetalol is effective in the treatment of essential hypertension, renal hypertension, pheochromocytoma, pregnancy hypertension and hypertensive emergencies. In addition, preliminary studies indicate that labetalol may be of value in the management of ischemic heart disease. The most troublesome side effect of labetalol therapy is posture-related dizziness. Other reported side effects of the drug include gastrointestinal disturbances, tiredness, headache, scalp tingling, skin rashes, urinary retention and impotence. Side effects related to the beta-adrenoceptor blocking effect of labetalol, including asthma, heart failure and Raynaud's phenomenon, have been reported in rare instances.
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PMID:Labetalol: a review of its pharmacology, pharmacokinetics, clinical uses and adverse effects. 631 May 29

Nineteen patients with uncomplicated essential hypertension and low activity of plasma renin in response to a change from recumbency to an upright posture along with furosemide administration were given spironolactone, 400 mg/d, or chlorthalidone, 100mg/d, in a double-blind, random-sequence, crossover trial. The sequence of treatments was placebo for 2 months, one active drug for 2 months, placebo again for 1 month and the other active drug for 2 months. With both active treatments the average systolic, diastolic and mean arterial pressures decreased significantly. The two agents were equally efficacious in lowering the blood pressure regardless of the severity of hypertension during placebo treatment. Body weight, 24--hour urinary excretion of sodium, the plasma renin activity and the plasma aldosterone level at the end of the initial placebo period did not allow us to predict the response to either drug. Both drugs reduced the body weight and increased the stimulated plasma renin level activity. Chlorthalidone significantly increased the serum uric acid level and significantly reduced the serum potassium level. Three patients experienced orthostatic dizziness during spironolactone therapy, but no adverse symptoms were observed with chlorthalidone therapy. Thus, spironolactone is an effective alternative to thiazide-type drugs in patients with low-renin essential hypertension.
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PMID:Comparison of chlorthalidone and spironolactone in low--renin essential hypertension. 633

The pharmacokinetics, clinical efficacy, and adverse effects of three calcium-channel blocking agents--verapamil, nifedipine, and diltiazem--are reviewed. Verapamil, nifedipine, and diltiazem are absorbed well after oral dosing, but absolute bioavailability of each is reduced substantially by a first-pass effect. Each drug is metabolized extensively (verapamil and diltiazem to moderately active metabolites) by the liver. A substantial percentage of each drug is bound to plasma proteins, but the binding is of clinical importance only for nifedipine (92--98% protein bound). Intravenous verapamil has become the agent of first choice for treatment of acute paroxysmal supraventricular tachycardia (PSVT); use of chronic oral verapamil therapy for prophylaxis remains controversial. Verapamil and diltiazem have been evaluated with mixed results for atrial flutter and fibrillation. For treatment of myocardial ischemia, calcium-channel blockers may be of some value (possibly in combination with nitrates of B blockers). All three agents have been studied in patients with exertional angina with good results. Calcium-channel blockers appear to be equal with nitrates for treatment of variant angina. Patients with hypertropic cardiomyopathy have been treated with verapamil and nifedipine with promising results. Nifedipine has been effective for treatment of essential hypertension. Adverse effects of calcium-channel blockers have been relatively minor or infrequent. Diltiazem overall has the best side-effect profile, with adverse effects causing discontinuation of therapy in about 2--10% of patients; verapamil in intermediate (8--10%) and nifedipine the worst (17%) in this respect. The most common side effects generally are fatigue, headache, dizziness, skin rash, and peripheral edema. While they generally should be reserved for patients in whom more conventional therapy has failed (except those with PSVT), calcium-channel blockers appear to have a valid role as reserve agents for exertional and variant angina, cardiomyopathy, and hypertension.
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PMID:Update on calcium-channel blocking agents. 635 66

Labetalol, a new alpha- and beta-adrenergic blocking agent, was administered to 57 patients with essential hypertension whose standing diastolic blood pressure was 105 to 120 mm Hg after three and four weeks of placebo therapy and greater than 90 mm Hg after three to four weeks of therapy with hydrochlorothiazide, 25 mg twice a day. Patients were then randomly assigned on a double-blind basis to receive either labetalol, 100 mg twice a day, or placebo combined with hydrochlorothiazide. Thereafter, the dose of labetalol was titrated weekly in both groups to a maximum of 400 mg twice a day to achieve a standing diastolic blood pressure of less than 90 mm Hg that was also decreased from the hydrochlorothiazide baseline by 10 mm Hg or more (therapeutic goal). Labetalol was abruptly discontinued after four weeks of treatment and patients were given hydrochlorothiazide alone for two additional weeks. After one week of labetalol therapy, 100 mg twice a day (added to hydrochlorothiazide), there was a significantly greater reduction in supine systolic/diastolic blood pressure (6/5 mm Hg, p less than 0.04/less than 0.03) and standing blood pressure (9/7 mm Hg, p less than 0.01/less than 0.01) than with placebo therapy (3/0.5 and 3/1 mm Hg, respectively). The blood pressure reduction in the labetalol-treated group was associated with a 4 and 5 beats per minute reduction in the supine and standing heart rates, respectively. The median labetalol dose required to achieve the standing diastolic blood pressure goal was 400 mg twice a day. After four weeks of labetalol treatment, the mean reduction in blood pressure from the hydrochlorothiazide baseline was 12/13 mm Hg (p less than 0.01/0.01) in the standing position and 8/8 mm Hg (p less than 0.01/0.01) in the supine position. These blood pressure reductions were accompanied by a mean reduction in heart rate of 7 beats per minute. The most frequently reported complaints other than thiazide-induced nocturia included dizziness, fatigue, nausea, rash, and/or pruritus. Most of these complaints were reported at a similar incidence while patients were receiving placebo or hydrochlorothiazide alone as when receiving labetalol with hydrochlorothiazide. After abrupt withdrawal of labetalol, no evidence of rebound hypertension was observed. Labetalol is a safe and effective step II drug when added to hydrochlorothiazide for the treatment of patients with moderate to moderately severe hypertension.
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PMID:Step II treatment with labetalol for essential hypertension. 635 2

1 Fifty-seven patients with mild or moderate essential hypertension, mean age 50 (range 31-69) were randomised to treatment with either captopril or atenolol. Twenty-six patients in each group completed the study. 2 Captopril (25-50 mg three times daily) and atenolol (50-100 mg once daily) caused a highly significant fall in blood pressure both supine and standing. 3 When hydrochlorothiazide (25-50 mg once daily) was added a further fall in blood pressure was observed in both groups. 4 Captopril as single drug caused no significant change in heart rate, while atenolol significantly reduced heart rate both supine and standing. 5 Two patients were excluded from the captopril group, one because of a reversible loss of taste and the other because of dizziness. Three patients were excluded from the atenolol group, two because of bradyarrhythmias and one because of inadequate blood pressure response. 6 Both captopril and atenolol were found to be effective antihypertensive agents, suitable for the treatment of essential hypertension.
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PMID:Captopril and atenolol combined with hydrochlorothiazide in essential hypertension. 675 91

1 The long-term effect of the converting-enzyme inhibitor captopril was investigated in 76 patients with various forms of severe hypertension, most cases being resistant to a standardised triple therapy (100 mg hydrochlorothiazide or 80-500 mg frusemide; 320 mg propranolol; and 200 mg hydralazine). 2 In each of the three groups examined (essential, renovascular, and renal parenchymatous hypertension) captopril led to a prompt and sustained reduction in systolic and diastolic blood pressure. Up to an observation time of 2 1/2 years patients with renovascular hypertension showed a more pronounced fall in mean diastolic blood pressures than those with essential hypertension. About 90% of all patients required a diuretic and a substantial percentage of patients needed propranolol as a third drug. 3 The most frequent side effects were skin manifestations, taste disturbances, dizziness, and non-productive cough. Serious adverse effects were rare and included one case of leucopenia and one of the nephrotic syndrome, both of them reversed after withdrawal of captopril. Further analysis showed that side effects occurred mainly in patients with impaired kidney function receiving relatively high dosages of captopril (greater than 200 mg/day). 4 Our results show that captopril is a very potent blood-pressure-lowering agent in severe hypertension, especially in cases with renovascular hypertension.
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PMID:Long-term experience with captopril in severe hypertension. 675 7


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