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

The hemodynamic mechanism of the hypotensive effect of propranolol was studied by quantitative radiocardiography in 8 patients with dialysis-resistant hypertension. Propranolol treatment brought about a decrease in mean arterial pressure and peripheral vascular resistances. The cardiac index was slightly reduced only in the early stage of the treatment. No significant difference was found between patients on treatments lasting longer than 3 months and patients with dialysis-controlled hypertension. The results show that propranolol can be used safely as the sole antihypertensive agent in patients with dialysis-resistant hypertension.
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PMID:Chronic hemodynamic effects of propranolol treatment in dialysis-refractory hypertension. 74 Jan 3

The patient, a manic depressive who was treated with lithium for three years, suddenly developed severe neurotoxicity and a glomerulonephritis-like syndrome. The author believes that the lithium toxicity was facilitated by hot weather with excessive sweating, gall bladder pathology with fever, and decreased water and salt intake. The patient improved except for a persistent hypertension. Propranolol not only improved the hypertension but alleviated a lithium-induced tremor as well.
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PMID:Severe neurotoxicity and lithium therapy. 74 6

We studied the antihypertensive effect of propranolol alone and in combination with diuretics in 13 patients with high, 18 with normal and nine with low-renin essential hypertension whose blood-pressure response to diuretics was previously established. Propranolol (160 mg daily) significantly lowered mean arterial pressure in high-renin (129 +/- 2.6 to 114 +/- 2.1 mm Hg) and normal-renin (131 +/- 2.7 to 119 +/- 3.5 mm Hg) patients but not in low-renin patients. A positive correlation (r = 0.36, P less than 0.05) between fall in pressure and fall in plasma renin activity occurred at this dose when the whole group was considered. An antihypertensive effect occurred in both high-renin and low-renin hypertension during large-dose (320 to 960 mg daily) propranolol therapy. This effect was independent of changes in plasma renin activity. The antihypertensive effects of propranolol and diuretics were additive in normal-renin and high-renin hypertension. These data suggest that propranolol's pressure-lowering activity is due to both renin-dependent and renin-independent effects.
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PMID:Proposed mechanisms of propranolol's antihypertensive effect in essential hypertension. 77 30

When plasma renin activity is related to sodium balance as evaluated from urinary sodium excretion, a physiological index of normality is obtained along with the ability to detect subtle variations in renin secretion. This has made it possible to correlate more closely the antihypertensive action of propranolol with the renin level. Propranolol reduced renin in all patients but did not lower blood pressure in low renin hypertensive states. It was dramatically effective in lowering blood pressure of high renin and some normal renin patients. Its antihypertensive effect was directly related to the pretreatment renin level and also to the absolute decrement in renin reduction achieved. This was true in malignant, renal, renovasular, and essential hypertension. Altogether, these findings point to the involvement of the renin-aldosterone axis in these hypertensive states. They suggest that a major component of the antihypertensive action of propranolol is consequent to an antirenin effect which is perhaps neurologically mediated. Accordingly, in addition to its therapeutic values, the response to propranolol may provide a pharmacological indicator of the renin involvement in essential hypertension and it also may be a useful adjunct for predicting surgical curability of renovascular hypertension.
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PMID:Propranolol, renin and hypertension: a review. 78 50

1. Propranolol was given to eight haemodialysed patients with resistant arterial hypertension for periods ranging from 6 to 16 months. 2. The treatment brought about an excellent control of blood pressure in all cases. 3. After withdrawal of propranolol plasma renin activity rose on average 40% compared with the value obtained during treatment. However, no significant relationship was found between the change in plasma renin activity and the change in the diastolic blood pressure. 4. Stopping propranolol resulted in a prompt rebound of arterial pressure toward pretreatment values. However, hypertension was always controlled on resuming drug treatment. 5. The results show that this form of hypertension can be controlled on a long-term basis with propranolol. However, the effect on blood pressure seems not to be mediated by suppression of renin secretion.
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PMID:Long-term propranolol treatment of resistant arterial hypertension in haemodialysed patients. 80 45

Minoxidil is a potent orally administered vasodilator under investigation for use in severe hypertension. Fifteen patients with moderate to severe hypertension refractory to conventional antihypertensive drugs were treated with minoxidil on an outpatient basis. Propranolol and furosemide were administered concomitantly to control reflex tachycardia and fluid retention. Good blood pressure control was achieved in all but one patient with the average supine mean arterial blood pressure falling from 140 mm Hg with conventional drugs to 106 mm Hg with minoxidil (P less than 0.0005). The major side effects of fluid retention (9/15), hirsutism (15/15), and tachycardia were adequately controlled in all but one patient. We conclude that minoxidil will be a valuable drug in the outpatient management of refractory hypertension.
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PMID:The outpatient treatment of refractory hypertension with minoxidil. 87 41

D,L-Propranolol given in single doses by gavage or s.c. injection to awake rats, always slowed the heart without affecting blood pressure. Doses of 0.2 mg/100 g injected twice daily lowered systolic pressure after 3 days in DOCA hypertensive but not in normotensive or spontaneously hypertensive rats. When chronic treatment with propranolol preceded the induction of DOCA hypertension, the pressure elevation attained 14 weeks later was less in treated than in untreated rats. Pressor responses to injected norepinephrine and to posterior hypothalamic stimulation were significantly larger in DOCA hypertensive rats that had been treated chronically with propranolol than in those that had not. These results suggest that propranolol's antihypertensive effects are unimpressive because they are simultaneously opposed by an enhanced cardiovascular responsiveness to pressor stimuli.
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PMID:Propranolol in DOCA hypertensive rats: development of hypertension inhibited and pressor responsiveness enhanced. 88 Sep 80

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


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