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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The urinary excretion of free noradrenaline (NA), adrenaline (A), dopamine (DA), the DA/NA ratio in the urine, plasma renin activity (PRA) and their mutual relationship were investigated in 71 patients suffering from different types of arterial hypertension. In spite of the fact that the mean values of excreted catecholamines, with the exception of pheochromocytoma, lie within the range of values found in healthy controls, certain differences were found in spectrum of excreted catecholamines. In patients with labile, malignant and renovascular hypertension and in pheochromcytoma the higher mean excretion of NA and the low DA/NA ratio was accompanied by the higher PRA in comparison with fixed benign essential hypertension. On the other hand, in hypertension with low PRA (essential hypertension with suppressed renin and Conn's syndrome) a low excretion of NA and high DA/NA ratio was found. There was a significant, if not even very close negative correlation between the PRA and DA/NA ratios both in recumbent and upright position. The rise of PRA on standing up was followed by an increased excretion of NA while the excretion of DA did not change or decreased. Hence the DA/NA ratio when standing up showed a decreasing tendency as compared with values when lying down. Application of the beta-blocker Inderal decreased the PRA and the blood pressure not only in juvenile hypertensive patients with hyperkinetic circulation but also in the early phases of renovascular hypertension. It thus appears that endogenous catecholamines, first of all the ratio between the renin-inhibiting DA and the renin-stimulating NA, participate as one of several factors in the regulation of secretion and of the plasma levels of renin not only in juvenile hypertensive patients with hyperkinetic circulation but also in other types of hypertension.
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PMID:Relationship between plasma renin activity and urinary catecholamines in various types of hypertension. 97 8

The effect of a potent inhibitor of platelet aggregation, BL-3459, on adrenaline-induced myocardial necrosis was investigated in beagle dogs. BL-3459, an alpha-adrenergic receptor blocking agent, phenoxybenzamine, and a beta-adrenergic receptor blocking agent, propranolol, were compared for their ability to modify the effects of adrenaline on platelet function, arterial blood pressure and myocardial damage. Adrenaline infusion led to a dose-related myocardial damage, elevation in arterial blood pressure, elevation in screen filtration pressure (SFP) and fall in platelet count. BL-3459 inhibited the elevation in SFP and the fall in platelet count as well as limiting the extent of myocardial damage. Phenoxybenzamine significantly modified all adrenaline-induced changes except the elevation in SFP. Propranolol had little effect alone and seemed to antagonize the beneficial effects of BL-3459 when the two drugs were combined. These results suggest that while other factors may also be involved, platelet aggregation and transient hypertension are correlated with the extent of adrenaline-induced myocardial necrosis observed in this model. A potent inhibitor of platelet aggregation, BL-3459, and the alpha-adrenergic receptor blocking agent, phenoxybenzamine, appear to afford protection against the observed pathological effects.
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PMID:The effect of a potent inhibitor of platelet aggregation, BL-3459, on adrenaline-induced myocardial necrosis in beagle dogs. 99 29

Minoxidil has a direct dilator effect on the systemic arterial smooth muscle. It is potentially an important drug in the treatment of systemic hypertension, especially when combined with beta blockade, which is used to control the associated tachycardia and increase in cardiac output. However, recent observations have suggested that minoxidil might cause pulmonary hypertension. Consequently, we examined the acute effect of monoxidil and propranolol, separately and in combination, on the pulmonary vasculature of the anesthetized dog and the awake calf during normoxia and hypoxia. In both species minoxidil reduced pulmonary vascular resistance. In the dogs this appeared to be the result of a direct action on the pulmonary vascular smooth muscle and in the cattle it was secondary to beta-receptor stimulation. Propranolol alone in the cattle increased the pulmonary pressor response to hypoxia. While we have not examined the possibility that chronic administration of minoxidil might cause pulmonary hypertension by some other mechanism, our acute studies suggest that it reduces, rather than increases, pulmonary vascular resistance. Furthermore, there seems to be a species difference in the mode of its action in dogs and cattle.
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PMID:Minoxidil reduces pulmonary vascular resistance in dogs and cattle. 99 42

Six patients with the diagnosis of acute mania were treated with high doses of the beta-adrenergic blocking agent propranolol. One of these patients was treated during two manic phases. Psychopathologic change during treatment was rated daily by a psychiatrist not informed on the patients medication. The IMPS (Inpatient Multidimensional Psychiatric Scale) was used. Three cases were placebo-controlled under double blind conditions. Four times we had a second medication period, twice with propranolol and once with oxprenolol and dexpropranolol respectively. Propranolol was administered every 4 h (six times per day), starting with single doses of 20-40 mg. Doses were increased individually under control of pulse rate, blood pressure, and ECG. Augmentation of doses was continued until an effect on manic symptomatology was undoubtedly seen or until therapy had to be discontinued because of side-effects. In four patients definite improvement of manic symptomatology could be achieved during altogether five manic phases within usually two treatment periods of 5-15 days. Manic behavior disappeared completely in two of these patients. The effective dosage of propranolol varied between 280 and 2320 mg per day. All of the improved patients relapsed after discontinuation of the drug. In the only case on dexpropranolol (5 days up to 900 mg daily) the effect was questionable. No extrapyramidal side-effects were observed. In one patient treatment was discontinued because of lack of cooperation, in another because of extrasystoles. Gastrointestinal bleeding occurred in the patient who received dexpropranolol. This complication was possibly due to other medication. Other side-effects were insomnia, hypertension, precordial pain, abdominal pain as well as the expected hypotension and bradycardia. The significance of these results regarding the catecholamine hypothesis of manic-depressive illness is discussed.
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PMID:[The effect of the beta-adrenergic blocking agent propranolol in mania (author's transl)]. 99 94

1. The effect of chronic administration of propranolol on the development and maintenance of severe renal hypertension in rats subjected to unilateral renal artery constriction was studied in relation to possible changes in peripheral PRA and the blood and tissue levels of propranolol. Propranolol was administered s.c. twice daily in doses of 1, 10 and 25 mg/kg, starting 2 days before operation. 2. Contrary to expectations, not only did the initial rise in systolic blood pressure become accelerated, but the established level of hypertension attained in the propranolol treated rats was of the same severity as that attained in placebo treated rats. Moreover, the progressive rise in peripheral plasma renin activity following unilateral renal artery constriction was not affected by propranolol administration. 3. The same doses of propranolol were also administered daily for 8 days to rats with established severe hypertension. A slight further rise in blood pressure occurred initially, followed by a moderate decrease of 15-25 mmHg. Propranolol failed to exert this minor hypotensive effect in hypertensive rats treated concomitantly with furosemide. No suppressive effect on the markedly increased levels of plasma renin activity was observed in these severely hypertensive rats in the presence or absence of furosemide administration. 4. These results indicate that in severely renal hypertensive rats propranolol has only a minor hypotensive effect and no blocking action on renin release under the conditions of study.
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PMID:Effects of propranolol on development and maintanance of severe renal hypertension in rats. 100 94

The paper presents the results of an examination of 62 patients with postinfarction cardiosclerosis by means of echocardiography and ultrasonic scanning. The impact of the asynergy zone on the development of cardiac insufficiency was studied with reference to the area of myocardial lesion. Myocardial hyperkinesia is characterized, its compensatory effect in postinfarction cardiosclerosis and arterial hypertension is discussed. The effect of Inderal and Ildomen on both the zones of hyperkinesia, and on the indices of cardiac haemodynamics as a whole is described.
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PMID:[Importance of myocardial asynergy zones in the development of cardiac insufficiency]. 101 9

1. In patients with mild or moderate essential hypertension, oral propranolol, given in incremental doses, produced a moderate but significant lowering of blood pressure which was correlated with the concentration of propranolol in plasma. 2. Propranolol also reduced plasma renin activity (PRA) in the supine posture, on standing and after intravenous frusemide. However, 'supine' and 'frusemide' PRA values were markedly reduced at a plasma concentration of propranolol that had little effect on blood pressure. 3. On administration of propranolol there was little correlation between blood pressure decrease and PRA suppression, and even less between pretreatment PRA values and hypotensive response. 4. It is concluded that in patients with mild and moderate hypertension and low or normal plasma renin activity, suppression of PRA is not an important determinant of the hypotensive response to propranolol.
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PMID:Hypotensive and renin-suppressing activities of propranolol in hypertensive patients. 105 79

1. Plasma renin activity (PRA) and renin dependency of the blood pressure was analysed in ten patients with various forms of hypertension before and during treatment with volume depletion and/or propranolol. Renin dependency was tested by infusion of the specific competitive angiotensin II antagonist Sar1-Ala8-angiotensin II (P113). 2. The P113-induced fall of the blood pressure did correlate with the log PRA (r=0-888, P less than 0-001). This correlation was found irrespective of different types of hypertension and treatment schedules. 3. During volume depletion, PRA was stimulated and renin dependency of the blood pressure increased. Propranolol therapy suppressed PRA during normovolaemia as well as during volume depletion, and this was accompanied by a decrease of the renin dependency. 4. No incication was found that a given PRA is of special importance for blood pressure elevation in different patients. 5. Suppression of PRA by propranolol is one of the anti-hypertensive mechanisms of this drug.
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PMID:Change in the renin dependency of blood pressure induced by volume depletion and/or propranolol therapy in hypertensive patients. 107 4

1. Propranolol, when used for treating arterial hypertension, may influence determinants of both cardiac and vascular function; the consequent changes in cardiac performance may result from the interaction of different and possibly opposite effects. 2. Cardiac funtion was investigated in fifty-four primary hypertensive men in the pretreatment state and after 3 weeks of propranolol therapy at a daily dose of 320 mg. 3. beta-Receptor blockade caused depression of pre-injection left ventricular function, which was unrelated to the direction and the extent of changes in peripheral circulation. 4. The ejection left ventricular function could be either depressed or improved depending on the direction to which treatment shifted the vascular resistance, and consequently, the impedance to left ventricular ejection. 5. Withdrawal of the adrenergic support is probably the major factor responsible for the poor ventricular adaptation to an augmented impedance.
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PMID:Cardiac function in the treatment of arterial hypertension with propranolol. 107 80

1. In a health examination survey of 2322 men, aged 49-50 years, the prevalence of hypertension was 7-5%. All men with a supine diastolic blood pressure greater than or equal to 105 mmHg were invited to a hypertension clinic. 2. Two years' treatment in eighty-six men achieved a blood pressure reduction of 31/16 mmHg, which was maintained for a 4 years period and considered satisfactory in 80% of the subjects. Propranolol was used in more than 80% of the cases. 3. The study indicates that it is possible to obtain acceptable blood pressure control in the community.
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PMID:Treatment of hypertension in middle-aged men: a feasibility study in a community. 107 87


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