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

Studies in 55 patients with benign essential hypertension showed that the beta-blockers bufuralol (22 patients) and propranolol (33 patients) at a dose ratio of 1:4, possess comparable antihypertensive efficacy despite different properties regarding intrinsic sympathomimetic activity. Beta-blocker-monotherapy normalized blood pressure ( less than 140/90 mm Hg) in one fourth of the patients. Body weight and plasma and blood volumes remained unchanged during beta-blockade of four to six weeks duration, the mean plasma potassium was slightly increased. The inhibition of plasma renin activity (PRA) was more pronounced with propranolol (-69%) than with bufuralol (-47%). Wirth both beta-blockers decreases in blood pressure correlated inversely with pre-treatment PRA (p less than 0.05). Propranolol-induced changes in blood pressure correlated also with associated changes in PRA (p less than 0.005); in contrast, no such relationship was observed with bufuralol. The blood pressure effects of bufuralol, however, correlated significantly with changes in urinary noradrenaline excretion (r=0.41; p less than 0.05). Patient sub-groups with low, normal or high pre-treatment PRA in the average showed a comparable pattern of pre-treatment noradrenaline excretion and patients with normal renin levels exreted more adrenaline than those with low renin levels (p less than 0.001). These data are consistent with the concept that in untreated essential hypertension PRA may be an index of adrenergic activiity, the latter representing an important determinant of blood pressure response to beta-blockade. The blood pressure lowering effects of bufuralol in benign essential hypertension seem to be independent of renin and may be related, at least partly, to diminished free peripheral noradrenaline levels.
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PMID:[Interrelations between blood pressure, blood volume, plasma renin and urinary catecholamines during beta-blockade in essential hypertension (author's transl)]. 0 63

Eleven beta-adrenergic receptor blocking agents and derivatives were evaluated for their ability to affect systolic arterial blood pressure and pulse rate in unanesthetized, male spontaneously hypertensive rats (SHRs) and normotensive Wistar Kyoto (WKY) controls. Animals ranged from 7 to 76 weeks of age. The subcutaneous injection of 5 and 45 mg/kg metoprolol in 52 to 64 week old SHRs and 45 mg/kg twice a day to 26 to 29 week old SHRs produced a significant decrease in blooc pressure. The subcutaneous injection of pindolol (0.1 and 1.0 mg/kg) produced a greater and more consistent depressor effect in mature SHRs. The subcutaneous administration of sotalol (100 mg/kg) and alprenolol (20 mg/kg) resulted in a depressor action which was significant 120 minutes after injection of the drug. In the doses used, propranolol, oxprenolol, 4-hydroxypropranolol and K9-1366 produced pressor effect in SHRs. Propranolol did not cause this pressor effect in prehypertensive (seven week old) SHRs. Practolol, dextro-propranolol and KO-1313 had no effect on blood pressure in the doses used. Propranolol, pindolol, metoprolol, dextro-propranolol, 4-hydroxypropranolol, practolol, oxprenolol, KO-1366 and KO-1313 produced no significant effects on blood pressure in normotensive WKY controls in the doses tested. Placing oral doses of 160 mg/kg/day of metoprolol in the drinking water for seven days significantly lowered blood pressure in 14 week old SHRs previously exposed to ineffective doses of 77 mg/kg/day for 24 days. The administration of oral doses of oxprenolol (40 mg/kg/day) in drinking water for three weeks had a slight but insignificant pressor effect. Smaller doses of metoprolol (15 and 39 mg/kg/day for three to four weeks) and practolol (70 to 85 mg/kg/day for two weeks) had no effect on 52 week old SHRs. Oral doses of pindolol, metoprolol, practolol and oxprenolol had no significant effect on blood pressure in WKY controls. There was no clear relationship between the effects of the drugs on blood pressure and their ability to affect the pulse rate. Similarly, there did not appear to be any consistent relationship between the potency of the beta-blocking drug and the blood pressure lowering action. In addition, neither cardioselective beta-blockade nor sympathomimetic properties allowed the prediction of blood pressure responses to the administration of those agents possessing these features. Although SHRs provide a valuable model of human essential hypertension, the variable effects reported here and elsewhere in the literature require caution as to the applicability and usefulness of testing and evaluating beta-adrenergic blocking drugs for theri potential anti-hypertensive effects in this particular form of experimental hypertension.
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PMID:Beta-adrenergic receptor blocking drugs in spontaneous hypertension. 1 Jul 29

The beta blocking agents are valuable drugs in cardiology. They are effective in any fast arrhythmia. Together with nitroglycerin, beta blockers are drugs of first choice in angina. As antihypertensives, they have advantages that should make them drugs of first choice. For migraine the beta blockers are equal to any other type of drug. With more study their place in treating anxiety will be clarified. And without question other uses will be found. It is difficult for this author to understand the attitude of the FDA to this class of drugs. To limit the American physician to only one drug in this large group of drugs is unheard of. Although it can be argued that propranolol is the best one, there are obvious cases where another drug would be better. For example, propranolol induces nightmares in a few patients. There is evidence to show that timolol does this less frequently. FDA delay in approval of propranolol for essential hypertension is totally incomprehensible. Other approved drugs are less effective and much more toxic. Propranolol, and the other beta blockers, are safe and effective. The adverse beta effects are easily controlled or avoided. The other adverse effects are no more frequent than with any other class of drugs, and all are reversible. It is to be hoped that science and common sense will prevail over bureaucratic indecision.
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PMID:Present state of alpha and beta adrenergic drugs III. Beta blocking agents. 1 53

Hemodynamic and renin studies at rest and during graded upright ergometry were performed in 21 patients with essential hypertension before and after propranolol. Beta-adrenergic receptor blockade reduced exercise-stimulated cardiac and renin responses significantly more when compared with the corresponding effects at rest. Propranolol increased peripheral resistance at rest but not during exercise. The degree of the individual hemodynamic changes after propranolol correlated better with the corresponding control values than with age or renin. A direct relationship between the percent reduction of heart rate and renin responses after acute beta-blockade indicates a parallel suppression of cardiac and renal receptor functions.
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PMID:[Exercise hemodynamics and renin before and after acute beta block in patients with essential hypertension]. 1 88

1. A Valsalva-like manoeuvre was used to elicit graded rises in total peripheral resistance (TPR) in conscious rabbits. The rises were reflex and mediated through sympathetic constrictors. Propranolol infused at different rates reaching plasma concentrations up to 240 (SEM 33) ng/ml had no effect on this reflex but reduced mean arterial pressure. However, the response was attenuated by clonidine in a dose-dependent manner. 2. Valsalva manoeuvres were used to elicit graded sympathetically mediated rises in TPR index in twenty-nine subjects with mean arterial pressure ranging from 75 to 165 mmHg. Absolute sensitivity of the constrictor response increased with rising resting TPR index, resulting in some enhancement of constrictor responses in the hypertensive subjects. It seems likely that non-autonomic factors (e.g. vessel structure) rather than hyperactive neural constrictor effects are involved in the enhanced constrictor responses in essential hypertension.
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PMID:Valsalva vasoconstrictor reflex in human hypertension in after beta-adrenoreceptor blockade in conscious rabbits. 1 55

1. The cardiovascular responses to handgrip exercise have been studied in ten patients with uncomplicated essential hypertension in a randomized crossover study of propranolol and prazosin. 2. Isometric handgrip exercise was performed with a calibrated strain gauge dynamometer at 30% of maximum voluntary contraction for 3 min. 3. Blood pressure and heart rate were measured in the supine position at rest and in the last 10 s of the exercise period. 4. These exercise studies were undertaken at the end of a run-in period and at the end of 1 month's optimal therapy with the two drugs. 5. The active treatment periods were separated by a 2 weeks placebo washout period. 6. Both drugs lowered the supine and standing systolic and diastolic pressures and there was no difference between these drugs in their effect on these variables. 7. Propranolol lowered the resting heart rate and neither drug suppressed the pressor response to isometric exercise. 8. The degree of pressure rise was similar with both drugs but propranolol suppressed isometric exercise-induced tachycardia.
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PMID:The effects of alpha- and beta-adrenergic receptor blockers on the pressure responses to isometric exercise in hypertensive patients. 4 50

To evaluate renal hemodynamic changes during therapy of essential hypertension, we treated 12 essential hypertensives in crossover fashion, with 1 month each of placebo, prazosin, and propranolol alone. During prazosin treatment, blood pressure was normalized with preservation of glomerular filtration rate, renal plasma flow, and renal blood flow. Propranolol, however, normalized blood pressure with an associated significant decline in glomerular filtration rate, renal plasma flow, and renal blood flow. The potential mechanisms are discussed.
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PMID:Renal perfusion changes during treatment of essential hypertension: prazosin versus propranolol. 9 38

The influence of the beta receptor blocking agent propranolol on plasma catecholamine concentrations was studied in eight patients with essential hypertension. The study was of single blind crossover design. Propranolol given in oral doses ranging from 60 to 240 mg daily for a period of 3 weeks decreased blood pressure and heart rate. The beta-adrenergic blocking agent caused plasma catecholamine levels to increase both at rest and during bicycle exercise. Chromatographical analysis showed that concentrations of noradrenaline as well as of adrenaline rose during treatment with propranolol. However, dopamine-beta-hydroxylase activity in plasma was not altered. Furthermore, the urinary excretion of noradrenaline, adrenaline and 4-hydroxy-3-methoxy mandelic acid did not change during beta receptor blockade. The results are compatible with the assumption that antihypertensive doses of propranolol by decreasing cardiac output cause an activation of the sympatho-adrenal system.
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PMID:Studies on the effects of propanolol on plasma catecholamine levels in patients with essential hypertension. 9 11

The hemodynamic changes observed in patients with the "hyperkinetic" form of borderline (labile) essential hypertension (BEH) could be related to the hyperresponsiveness of cardiac beta-adrenergic receptors to catecholamines. The isoproterenol-induced increase in plasma cyclic adenosine 3':5'-monophosphate (cAMP) reflects the response of adenylate cyclase to beta-adrenergic stimulation, whereas a non-beta-receptor-mediated increase occurs with the administration of glucagon. Both substances were infused into 13 control subjects and 14 patients with the hyperkinetic form of BEH before and after propranolol administration. Baseline plasma cAMP concentrations were comparable in both groups. After 30 minutes of isoproterenol infusion (20 ng/kg per min) a significantly higher increase in plasma cAMP and heart rate and a smaller decrease in diastolic blood pressure were seen in this type of BEH than in control subjects. The increase in plasma cAMP and in heart rate correlated positively when all subjects were considered together. Propranolol abolished hemodynamic and humoral responses to a similar degree in both groups. The plasma cAMP responses to glucagon (200 ng/kg per min) were slightly lower in our patients with BEH than in control subjects and were not suppressed by propranolol. The data are compatible with a hyperreactivity of the beta-adrenergic receptors or of the adenylate cyclase or both in hyperkinetic BEH and could correspond to the previously observed exaggerated beta-adrenergic drive to the heart in this type of hypertension. The non-beta-receptor-mediated rise in plasma cAMP (glucagon), however, remains comparable in control subjects and BEH.
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PMID:Plasma cyclic adenosine 3':5'-monophosphate response to isoproterenol and glucagon in hyperkinetic borderline (labile) hypertension. 17 67

Maximal exercise test was performed in 15 patients with essential hypertension before and after 10 days of treatment with oral propranolol in daily doses of 320 mg. After the treatment, heart rate, and systolic and diastolic blood pressure significantly fell both at rest and after the test; a greater, though not significantly, workload was tolerated; a significant decrease was observed in the product of heart rate and systolic blood pressure, together with a marked reduction in electrocardiographic ischemic changes. Propranolol treatment, besides being an effective antihypertensive agent, improved ischemic changes induced by exercise and cardiac performance in hypertensive patients, also in the presence of left ventricular hypertrophy.
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PMID:Maximal exercise test in patients with essential hypertension treated with propranolol. 35 99


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