Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Amlodipine, a novel dihydropyridine calcium-antagonist, was compared to slow-release nifedipine in a short-term study on 40 patients with mild to moderate essential hypertension, in order to assess the efficacy and tolerability of two different dihydropyridine calcium-antagonists with short and long half-life. After a two-week single-blind placebo period, patients were given, in a randomized sequence, amlodipine (5 or 10 mg/day od, 20 patients) or nifedipine s.r. (20 or 40 mg BID, 20 patients). At the end of treatment (12 weeks) a significant lowering of arterial pressure was obtained after 24h from the administration of amlodipin (-34/-17 mmHg) and after 12h from the administration of nifedipine s.r. (-33/-16 mmHg). Furthermore, with both drugs, no significant changes in heart rate and ECG have been reported. Amlodipine was better tolerated than nifedipine, as shown by the lower incidence of side effects. Therefore amlodipine proved to be an effective and well tolerated drug in the therapy of mild to moderate hypertension.
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PMID:[A comparison between amlodipine and nifedipine retard in patients with essential arterial hypertension]. 153 44

A total of 203 patients with hypertension (supine diastolic blood pressure of 100-119 mm Hg) from six centers entered into a 3-week placebo baseline followed by 5 weeks of active treatment (either placebo or isradipine 2.5, 5, 7.5, or 10 mg BID) to determine the effectiveness of isradipine on blood pressure control. Electrocardiographic criteria for left-ventricular ischemia were coded blindly using the Minnesota Codes 4-1 to 4-4 and 5-1 to 5-3 at the end of baseline and active treatment periods. One hundred seventy patients with hypertension and matching and complete electrocardiograms completed the study for analysis: 63 (37%) were white and 117 (69%) were men. They were 52.1 +/- 10.3 years old mean +/- SD; range: 22-77 years). No myocardial infarction occurred during the active phase. Fifty-eight of 170 (34%) at baseline and 54 of 116 (32%) at week 5 had left atrial enlargement. Romhilt-Estes left-ventricular hypertrophy was not significantly different at baseline versus active treatment: 14 of 170 (8.2%) versus 15 of 170 (8.8%). At baseline, the rate of active ischemia was 28.2% (48/170): 27.8% (10/36) were randomized to receive placebo during active treatment and 28.4% (38/134) were given isradipine (P = NS). For those without ischemia at baseline, the rate of change to electrocardiographic ischemia during active treatment was 0% (0/26) for those receiving placebo and 3.1% (3/96) for those taking isradipine (P = NS). For those with ischemia at baseline, the rate of change to no ischemia during active treatment was 20% (2/10) for those receiving placebo and 10.5% (4/38) for those taking isradipine (P = NS).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Assessment of electrocardiographic ischemia in hypertensive patients treated with isradipine or placebo. 182 11

A double-blind parallel group study was conducted to examine the effects of oral labetalol, in doses from 100 to 800 mg BID, and propranolol, 40 to 320 mg, in patients with mild to moderate hypertension. The doses of labetalol (n = 74) and propranolol (n = 79) were titrated weekly to achieve a sitting diastolic blood pressure (DBP) of less than 90 mmHg or at least a 10-mmHg decrease from placebo baseline on two consecutive visits. A 2-month fixed-dose maintenance phase followed in which a diuretic could be added if the sitting DBP was greater than or equal to 100 mmHg on maximum doses of either drug. BP and heart rate were measured 8-12 hours after a dose in the sitting and standing positions. Labetalol was significantly more effective at the end of monotherapy than propranolol was in lowering both the sitting (p less than .05) and standing (p less than .04) DBP. The reduction in the systolic, although more pronounced for those on labetalol, was not significantly different; 53% of patients had a "good" response to labetalol compared with 30% of the propranolol group. Propranolol significantly (p less than 0.01) lowered heart rate compared with labetalol. Nine patients in the labetalol group and 10 in the propranolol group required a diuretic. The decrease in BP after the addition of a diuretic was comparable. Changes in plasma lipids were not significant, but HDL increased 9% with labetalol and decreased 2% with propranolol. Triglycerides increased 25% with labetalol and 31% with propranolol.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Labetalol compared with propranolol in the treatment of black hypertensive patients. 331 2

Fifty-two asthmatic patients with mild to moderate hypertension were screened for bronchosensitivity to propranolol in a double-blind randomized fashion after a 2-week minimum placebo run-in period. Thirty-five patients qualified on the basis of a decrease in 1-second forced expiratory volume FEV1 by greater than or equal to 20% after 80 mg of propranolol with no more than a +/- 15% change after placebo. Of these patients, 18 were then randomly assigned to antihypertensive treatment with labetalol at doses that were increased at weekly intervals (100, 200, 400, 600 mg BID) and 17, with hydrochlorothiazide (HCTZ) (25 or 50 mg BID) as needed for control of hypertension. At each placebo washout visit and at each of the four active drug-treatment phase visits, spirometric measurements were obtained just prior to the morning dose of medication and again 2 hours later on the initial visit (i.e., following the initial dose of active treatment) and on each visit when the dosage was increased. Neither HCTZ nor labetalol (average daily doses at the end of the study were 88 and 555 mg, respectively) caused bronchoconstriction: Mean FEV1 did not change from the baseline neither prior to the morning dose (evaluation of the "chronic" treatment effect) nor 2 hours after dosing (evaluation of "acute" treatment effect). Three patients in each treatment group reported increased dyspnea and two on labetalol and one on HCTZ had increased wheezing; the mean weekly isoproterenol usage per patients was similar for the two treatments (1.3 times/week/pt for labetalol and 1.6 times/week/pt for HCTZ).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of treatments with labetalol and hydrochlorothiazide on ventilatory function of asthmatic hypertensive patients with demonstrated bronchosensitivity to propranolol. 383 97

The antihypertensive effect of oral labetalol and propranolol were evaluated in 65 black and 75 white patients with mild to moderate hypertension (standing diastolic blood pressure (StDBP) of 90-115 mmHg) in a double-blind multicenter clinical trial. Following a 4-week placebo phase, labetalol (n = 70) or propranolol (n = 70) was randomly assigned. During a 5-week titration phase, labetalol could be increased from 100 mg BID to 600 mg BID to achieve a StDBP of less than 90 mmHg and a decrement of greater than or equal to 10 mmHg. Propranolol could be titrated from 40 to 240 mg BID. A 3-month maintenance phase was followed by an optional 8-month maintenance phase. Hydrochlorothiazide (HCTZ) could be added at any time during the maintenance phase. Supine and standing blood pressures were measured at each visit. Statistical analysis revealed significant (ANOVA, p less than 0.05) treatment by race effects. Therefore, the treatment groups were stratified retrospectively by race. This study demonstrated that labetalol is equally effective in white and black patients, whereas, propranolol is significantly (p less than 0.05) more effective in white than in black patients. Moreover, labetalol is significantly more effective than propranolol in lowering the standing systolic/diastolic blood pressure of black patients (p less than 0.02/p less than 0.001). These blood-pressure effects were accompanied by a significantly greater (p less than 0.04) reduction in heart rate with propranolol. Furthermore, significantly more (p less than 0.05) black patients treated with propranolol compared to those treated with labetalol required the addition of a diuretic for control of their blood pressure.
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PMID:Monotherapy with labetalol compared with propranolol. Differential effects by race. 391 17

Guanabenz, a centrally acting antihypertensive (alpha-agonist) that does not induce secondary sodium retention or other metabolic disturbances, was evaluated for up to two years at 19 investigational sites. In 329 patients completing six months of therapy, the mean supine diastolic blood pressure (SDBP) fell from 101 to 90 mmHg (P less than 0.01). Clinically significant individual SDBP decreases occurred in 74% of the patients by week 2, and these reductions were maintained in 72% at six months. Mean weight was reduced 1.4 lb (P less than 0.01), and mean supine pulse rate was decreased 5 beats/min (P less than 0.01). The most frequent effective doses were 8 and 16 mg BID (range, 2 to 32 mg BID). Principal side effects, usually mild, were sedation (31%), dry mouth (24%), dizziness (6%), and weakness (6%). Postural hypotension, impotence, and abrupt discontinuation symptoms were rare or absent. There were no clinically significant drug-related laboratory changes other than a 10 mg/100 ml mean serum cholesterol decrease. Two hundred twenty-two patients completed one year of therapy, and 80 completed two years, with little change in any parameters other than improvement in mean SDBP to 85 mmHg and in individual response rate to 84%. These results suggest that guanabenz is safe and effective for initial and sole therapy of hypertension.
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PMID:Long-term therapy of hypertension with guanabenz. 730 37

Neurohormonal activation with increased plasma renin activity and norepinephrine and vasopressin levels is characteristic of congestive heart failure and contributes to further decompensation and poor prognosis. We treated 20 such patients with the centrally acting sympathoinhibitory drug clonidine 0.15 mg BID and obtained hemodynamic measurements by cardiac catheterization and plasma neurohormone levels before and 2 to 3 hours after the first dose; in 7 patients, these measurements were taken again after 1 week of therapy. The initial dose produced significant decreases of 8% in mean arterial pressure, 23% in right atrial pressure, 21% in pulmonary capillary wedge pressure, 19% in mean pulmonary artery pressure, and 12% in heart rate, a 17% increase in stroke volume; and no significant changes in cardiac output and systemic vascular resistance. All changes remained virtually constant after 1 week. Plasma norepinephrine decreased by 28% after the initial dose and 62% after 1 week (P < 0.1), whereas plasma renin activity remained essentially unchanged. Plasma vasopressin tended to increase, its levels being inversely correlated with those of posttreatment norepinephrine (r = -.48 P < .03). Patients with baseline norepinephrine levels > 0.400 ng/mL has significantly poorer baseline hemodynamic parameters and tended to show more improvement with clonidine, although their data remained significantly worse than patients whose baseline norepinephrine was within the normal range. Sympathetic suppression with clonidine in congestive heart failure reduces preload, heart rate, and arterial pressure, all indexes of myocardial energy demand; the lack of significant reduction in systemic vascular resistance and increase in cardiac output might be attributable in part to enhanced release of vasopressin.2+ f2p4
Hypertension 1995 Nov
PMID:Suppressing sympathetic activation in congestive heart failure. A new therapeutic strategy. 862 Dec 15

Endothelin-1 infusion into humans to obtain pathophysiological plasma levels causes mild hypertension, strong renal vasoconstriction, and sodium retention. We studied whether oral use of the angiotensin-converting enzyme inhibitor enalapril (20 mg BID) or the calcium channel blocker nifedipine (60 mg OD) could attenuate these effects of endothelin-1 (2.5 ng/kg per minute for 90 minutes) in six healthy volunteers. Endothelin infusion alone increased plasma endothelin from 3.0 +/- 0.3 to 8.8 +/- 1.0 pmol/L (P < .05). Blood pressure rose by approximately 6 mm Hg (P < .05). Renal function changes were relatively large: Renal blood flow decreased from 941 +/- 76 to 729 +/- 118 mL/min (P < .05) and glomerular filtration rate from 105 +/- 9 to 92 +/- 10 mL/min (P < .05); renal vascular resistance increased from 101 +/- 7 to 152 +/- 20 mm Hg.min/L (P < .05); and sodium excretion decreased from 158 +/- 54 to 86 +/- 27 mumol/min (P < .05). Enalapril treatment reduced blood pressure from 94 +/- 2 to 87 +/- 3 mm Hg (P < .05) and prevented the hypertensive response to endothelin. By contrast, despite renal predilatation, endothelin reduced renal blood flow strongly (from 1063 +/- 127 to 763 +/- 100 mL/min, P < .05), although maximal renal vascular resistance was numerically lower (124 +/- 11 mm Hg.min/L) than during endothelin alone (P < .05). Glomerular filtration rate fell from 118 +/- 11 to 108 +/- 11 mL/min (P < .05). Enalapril did not alter the antinatriuretic effect of endothelin.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1995 Apr
PMID:Effectiveness of enalapril versus nifedipine to antagonize blood pressure and the renal response to endothelin in humans. 772 6

A prospective cross-over study was performed in a general practice environment to assess and compare compliance data obtained by electronic monitoring on a BID or QD regimen in 113 patients with hypertension or angina pectoris. All patients were on a BID regimen (nifedipine SR) during the first month and switched to QD regimen (amlodipine) for another month. Taking compliance (i.e. the proportion of days with correct dosing) improved in 30% of patients (95% confidence interval 19 to 41%, p < 0.001), when switching from a BID to a QD regimen, but at the same time there was a 15% increase (95% confidence interval 5 to 25%, p < 0.02) in the number of patients with one or more no-dosing days. About 8% of patients had a low compliance rate, irrespective of the dosage regimen. Actual dosage intervals were used to estimate extent and timing of periods with unsatisfactory drug activity for various hypothetical drug durations of action, and it appears that the apparent advantage of QD regimen in terms of compliance is clinically meaningful only, when the duration of activity extents beyond the dosage interval in all patients.
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PMID:[Time of drug intake in hypertension and angina pectoris. A controlled monitoring study]. 793 74

Isradipine is a dihydropyridine calcium-entry blocker. Previous controlled and blinded trials have demonstrated the safety and efficacy of isradipine in lowering blood pressure in patients with hypertension. The purpose of this study was to reassess this safety and efficacy in a large number of patients in an open-label, long-term, multicenter trial. A total of 501 patients with essential hypertension (diastolic blood pressure 95 to 114 mm Hg) received 5 to 10 mg/d of isradipine in two divided doses for a period of 32 weeks. The mean dose used was 7.4 mg/d with titration at week 4 from 5 mg/d (2.5 mg BID) to 10 mg/d (5 mg BID) if the diastolic pressure was still > 90 mm Hg. After 32 weeks of isradipine treatment, systolic blood pressure decreased from 154.9 +/- 16.4 mm Hg to 140.2 +/- 13.9 mm Hg (P < 0.001) and diastolic pressure from 101.2 +/- 5.2 mm Hg to 86.6 +/- 7.9 mm Hg (P < 0.001). This monotherapy was successful in reducing diastolic blood pressure > 10 mm Hg in 62.5% of the patients. Significant adverse effects were noted in 92 (18.4%) of the 501 patients; only 30 (6.0%) withdrew from the study because of adverse events. In this large, long-term, community-based study, isradipine was effective and well tolerated in most patients.
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PMID:A large, prospective, open-label study of isradipine in patients with essential hypertension. The Isradipine Investigators Group. 798 52


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