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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This review summarizes the available medical literature about plasma norepinephrine, which as been used as an indicator of sympathetic neural activity in clinical cardiology. Plasma norepinephrine levels are elevated myocardial infarction and congestive heart failure, and the norepinephrine concentration varies with severity of disease. Patients with ischemic heart disease at rest show essentially normal plasma norepinephrine, but no studies have assessed norepinephrine levels during spontaneously occurring typical angina pectoris. Plasma norepinephrine also is increased during hypertension occurring after coronary bypass surgery or repair of aortic coarctation. Propranolol increases plasma norepinephrine, and acute withdrawal of propranolol does not. Sodium restriction increases plasma norepinephrine in healthy persons, but no information is available about its effect on patients with congestive heart failure. Insufficient data are available to make strong inferences about sympathetic activity in cardiomyopathy, essential hypertension or pulmonary hypertension, and little or no information is available about plasma norepinephrine in ventricular fibrillation without myocardial infarction, the mitral valve prolapse syndrome, digoxin effect, syndromes associated with prolonged electrocardiographic Q-T interval and the hyperkinetic heart syndrome.
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PMID:Plasma norepinephrine as an indicator of sympathetic neural activity in clinical cardiology. 617 Nov 57

The antihypertensive effect of debrisoquine (20 mg/day), methyldopa (100 mg/day) and propranolol (160 mg/day) was compared to that obtained with a placebo in a controlled trial carried out by a group of 14 internists. Forty-eight patients with uncomplicated essential hypertension were included. Mefruside (25 mg/day) was first given alone for 6 weeks ("open phase" of the trial) and to this diuretic was then added in double-blind fashion and randomized sequence a placebo or an active drug. Each of the 4 blind phases lasted 4 weeks. At the end of the "open phase", blood pressure in seated position averaged 168/111 +/- 19.6/13.5 mm Hg (mean +/- SD). A significant blood pressure decrease was observed after 4 weeks of treatment with the placebo as well as with the investigated compounds. With the placebo blood pressure was reduced to 158/102 +/- 19.6/13.5 mm Hg (p less than 0.001). The magnitude of the additional blood pressure decrease induced by the active drugs was relatively small and varied from 4 (debrisoquine) to 10 mm Hg (methyldopa, p less than 0.01) for the systolic and from 3 (debrisoquine, p less than 0.05) to 5 mm Hg (propranolol, p less than 0.05) for the diastolic. The percentage of patients with systolic pressure of less than or equal to 140 mm Hg and with diastolic pressure of less than 90 mm Hg during administration of either drug was not greater than 40 to 20% respectively. Propranolol appeared to be better tolerated than the other antihypertensive agents. These rather disappointing blood pressure results suggest that the efficacy of antihypertensive agents in private practice cannot be extrapolated from studies carried out in specialized hypertension clinics.
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PMID:[Evaluation by practicing physicians of the antihypertensive efficacy of debrisoquin, methyldopa and propranolol]. 634 33

This report describes a double-blind, parallel, comparative study of trimazosin (+/- polythiazide) and propranolol (+/- polythiazide) in 130 patients with essential hypertension. Both treatment regimens were shown to be effective in achieving statistically significant sustained reduction in blood pressure. Propranolol alone was somewhat more effective, at the doses selected, than trimazosin alone, but the hypertension of nonresponders in each treatment group was effectively controlled by the addition of low doses of polythiazide. Trimazosin had no effect on heart rate, whereas propranolol significantly lowered resting heart rates, which was occasionally troublesome. Side effects were less frequent in the trimazosin-treated group. Trimazosin lowered serum creatinine and blood urea nitrogen, an effect significantly different from that of propranolol. There was also a tendency for serum uric acid to rise in patients receiving propranolol and fall in those receiving trimazosin; polythiazide significantly raised uric acid levels. The effects of trimazosin and propranolol on the lipid profile were small, but the difference between the increase in the high-density lipoprotein-cholesterol fraction in trimazosin-treated patients and the decrease in propranolol-treated patients was significant and thought to be of interest.
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PMID:Double-blind comparison of trimazosin and propranolol in essential hypertension. 635 54

In a double-blind study, patients with moderate to severe essential hypertension were treated randomly with either indoramin or propranolol orally. The dose of both drugs was increased as necessary, to a predetermined level, in order to reduce the diastolic (Phase V) blood pressure to 100 mmHg or less. Patients were followed up for 12 weeks. There were 23 patients on propranolol and 27 on indoramin. The blood pressure in 22 patients on propranolol and 25 patients on indoramin was satisfactorily controlled in both the supine and standing positions. Mean supine blood pressure decreased from 181.3 +/- 14.2/116.2 +/- 6.8 mmHg to 140.6 +/- 7.1/95.7 +/- 3.6 mmHg after 12 weeks of treatment in patients receiving propranolol and from 188.3 +/- 18.9/118.4 +/- 8.7 mmHg to 144.7 +/- 7.3/95.7 +/- 2.5 mmHg in those treated with indoramin. There were no significant differences between the effects on supine and standing blood pressures and blood pressure control was maintained throughout the 12-week period in patients receiving indoramin and those receiving propranolol. Propranolol reduced the mean heart rate by approximately 16 beats/min in both the supine and standing positions. The maximum effect was seen 4 weeks after starting treatment and was maintained throughout the study. Sinus bradycardia (heart rate less than 60/min) occurred in 9 (39%) patients receiving propranolol. Indoramin caused a small but significant reduction in mean heart rate of approximately 4 beats/min in both the supine and standing positions. The maximum effect was seen after 2 weeks of treatment and was maintained for the rest of the duration of treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A double-blind comparison of indoramin and propranolol in the treatment of moderate to severe essential hypertension. 636 63

Eight out-patients with essential hypertension participated in a comparative, placebo-controlled study with a cross-over design. Pindolol and propranolol were administered orally in doses of 20.0 +/- 3.13 mg/d (mean +/- SEM) and 125.0 +/- 19.17 mg/d respectively. Pindolol reduced mean blood pressure by 11.9 mmHg; pre-ejection period index by 8.1 msec; total peripheral resistance by 3.1 mmHg min/L; and limb vascular resistance by 3.28 mmHg min 100 g/ml. Heart rate, cardiac output, plasma renin activity and urinary norepinephrine excretion rate were not altered by pindolol. Propranolol reduced mean blood pressure by 14.0 mmHg; heart rate by 9.1 beats/min; cardiac output by 0.57 L/min; limb blood flow by 1.06 ml/100 g.min; and plasma renin activity by 1.44 ng/ml/h; and increased pre-ejection period index by 8.7 msec. Total peripheral resistance, limb vascular resistance and urinary norepinephrine excretion rate were not altered by propranolol. It was concluded that: (1) the drugs, pindolol and propranolol, are equally effective as antihypertensive agents; (2) heart function and plasma renin activity are decreased by propranolol and unaltered by pindolol; (3) total peripheral resistance is decreased by pindolol and unaltered by propranolol; and (4) these findings may be explained by the intrinsic sympathomimetic activity exhibited by pindolol only.
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PMID:A comparative study on the effects of pindolol and propranolol on systemic and cardiac haemodynamics in hypertensive patients. 638 72

The effects of epinephrine (E) on plasma norepinephrine (NE) concentrations and cardiovascular responses before and after beta-blockade were studied in 36 patients with essential hypertension and 10 age-matched normal controls. The resting plasma NE and E were significantly higher in the borderline hypertensives (251 +/- 21 (SE) pg/ml, p less than 0.005; 57 +/- 5, p less than 0.05) than in normal controls (127 +/- 18; 38 +/- 7). An immediate rise in plasma E and NE was observed after one bolus intravenous administration of glucagon (1 mg). Then, plasma E fell rapidly to the baseline, whereas plasma NE declined much slowly. Propranolol did not affect the plasma E response to glucagon, but eliminated a prolonged rise of plasma NE. Exogenous E infusion (1.25-1.50 micrograms/min) for 30 min caused a definite rise in both plasma NE and blood pressures and lasted more than 30 min after termination of the infusion. Propranolol did not alter the time course of plasma E, but again inhibited a prolonged rise in both plasma NE and blood pressures. These findings support the view that plasma E can act physiologically as a sustained stimulator to the presynaptic beta-adrenoceptors, leading to an enhancement of NE release and a rise in blood pressure in man.
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PMID:The role of epinephrine in essential hypertension. 663 77

Atenolol, Pindolol and Propranolol in single daily doses administered to 18 selected patients with mild essential hypertension achieved adequate control of blood pressure. Chlorothiazide had been initially administered twice a day without full control of blood pressure and this diuretic therapy was continued unaltered throughout the study. Methacholine challenge testing of respiratory function was performed during the placebo phase and with each beta adrenoreceptor-blocking drug. In the 18 non-asthmatic patients, the reduction in FEV1, was significant only for propranolol therapy when compared to placebo. Each beta adrenoreceptor-blocking drug was associated with small, but significant, increases in fasting plasma triglyceride concentrations and suppression of fasting immuno-reactive glucagon concentrations.
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PMID:Beta adrenoreceptor-blocking drugs once daily in essential hypertension: a comparison of propranolol, pindolol and atenolol. 701 82

The effect of a propranolol-hydrochlorothiazide combination tablet was compared with the effects of its two components alone in the twice-daily treatment of mild to moderate essential hypertension (100 to 125 mmHg diastolic blood pressure). Propranolol alone or in combination was given at 80, 160, 240, or 320 mg/day; hydrochlorothiazide, at 50 mg/day. After a 3-week placebo period, a 12-week single-blind dose-finding test with the combination was held: 149/158 (94%) patients had decreases greater than or equal to 10 mmHg in diastolic blood pressure. Mean systolic and diastolic pressures were reduced by 26.6 mmHg 917%) and 19.2 mmHg (18.6%), respectively (P less than 0.001). A 10-week double-blind parallel treatment test followed, in which patients were assigned by random code to combination tablet, propranolol, or hydrochlorothiazide. There were significantly larger increases (P less than 0.05) in mean systolic or diastolic pressure with each component than with the combination from the end of dose-finding to each of the last four biweekly visits, to the mean of those four visits, and to the endpoint (last visit). The mean increases in pressure at the endpoint evaluation were (systolic/diastolic): combination (n = 47), 3.0/1.5 mmHg; propranolol (n = 51), 10.2/6.3 mmHg; hydrochlorothiazide (n = 52), 13.1/9.3 mmHg. During the double-blind period, no significant differences were demonstrated between the proportions of patients in each treatment group reporting new complaints. This study showed the combination to be as safe as, and more effective than, either component given at the same dose strength.
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PMID:Propranolol-hydrochlorothiazide combination in essential hypertension. 704 37

Pulmonary function was measured serially in two separate randomized trials of pindolol in the treatment of essential hypertension. Patients with overt obstructive airways disease were excluded. In study 1, 131 hypertensive patients were randomized to placebo (31) and 15 mg (33), 30 mg (33), and 60 mg (34) of pindolol. Pulmonary function was measured before and at weeks 8 and 15 of active medication. Bronchospasm--a 20% increase in forced expiratory volume in 1 second (FEV1) after isoprenaline--developed in three patients on active treatment and one on placebo. In eight patients on pindolol and one on placebo, bronchospasm ceased. Compared to placebo, no deterioration in pulmonary function occurred with pindolol and in three tests--maximum voluntary ventilation (MVV) (L/min), MVV%, midexpiratory flow rate (MEFR) (L/min)--significant improvement occurred. In study 2, 14 hypertensive patients were randomized to pindolol (mean dose 50 mg/day), 15 to propranolol (mean 360 mg/day), and 14 to chlorthalidone (mean 107 mg/day). Pulmonary function was measured after 3 weeks of placebo and again after 6 weeks of active treatment. While propranolol produced slight deterioration in pulmonary function, pindolol and chlorthalidone produced slight but significant improvement (p less than 0.05) with maximum MEFR (L/sec). Pulmonary function tests measured after isoprenaline were significantly worse in patients on propranolol compared to those on placebo, but were unchanged in patients on pindolol or chlorthalidone. The conclusions are: (1) Pindolol in antihypertensive doses does not produce airways obstruction and some improvement in pulmonary function may occur. (2) In comparable doses, pindolol has a positive effect on pulmonary function and propranolol a negative effect which, when summated, is statistically significant. (3) Propranolol, but not pindolol, appears to block the bronchodilator effects of isoprenaline. The lack of pulmonary function impairment may be due to intrinsic sympathomimetic activity properties of pindolol.
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PMID:Pulmonary function in hypertensive patients treated with pindolol: a report of two studies. 704 80

Although propranolol administration produces a lowering of PRA, PAC does not decrease in a similar fashion. In the present study the effects of propranolol on the aldosterone MCR were examined. Eight patients with essential hypertension were studied while receiving treatment with a diuretic and again after propranolol (160 to 320 mg/day) was added to the therapeutic regimen. Propranolol therapy was associated with a 25% decrease in PRA (p less than 0.05) and changes in PACs that were variable but not significantly different from diuretic therapy alone. The aldosterone MCR decreased from 1420 +/- 120 to 1120 +/- 90 L/24 hr in response to propranolol (p less than 0.01). The average production rate of aldosterone (MCR X PAC) did not change after propranolol treatment despite a decrease in PRA. There were no changes in plasma concentrations of potassium or in ACTH secretion (as reflected by levels of cortisol) to explain a role for propranolol to sustain aldosterone secretion. Thus propranolol administered to hypertensive patients pretreated with a diuretic can affect circulating levels of aldosterone apart from changes in PRA. Propranolol therapy produces a moderate reduction in aldosterone MCR and appears to augment aldosterone production by a mechanism exclusive of known stimuli.
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PMID:Effects of propranolol on aldosterone plasma concentration and aldosterone metabolic clearance in hypertensive patients. 736 15


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