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

The blood pressure responses following infusions of angiotensin II (ANG II) into the brain ventricles (i.v.t.) have been tested in spontaneously hypertensive (SH) rats and in normotensive Wistar Kyoto (WK) rats. The mean arterial blood pressure increases were significantly higher in SH rats than in WK rats. Propranolol treatment reduced blood pressure increases to i.v.t. ANG II in WK, but not in SH rats. The higher sensitivity to i.v.t. ANG II in SH rats supports a role of central ANG II in the maintenance of high blood pressure in SH rats.
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PMID:Increased blood pressure responses to central angiotensin II in spontaneously hypertensive rats. 73 52

By a combined vasodilator-[diisopropylamine (disostat), dihydralazine (depressan)] furosemide- (furesis-) infusion therapy was tried to achieve a new stabilisation of the blood pressure of therapy-refractory patients with hypertension. Propranolol (Obsidan) was additionally administered for the suppression of a sympathetic counter-regulation. On 3 patients is demonstrated how by a ten days' intensive decrease of the blood pressure and decrease of the extracellular fluid volume the therapy resistance may be interrupted and a repeated response to an oral antihypertensive standard therapy may be achieved.
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PMID:[Drug-induced readjustment of therapy-resistant hypertension]. 73 53

In 19 patients with arterial hypertension the hemodynamics were determined with a Swan-Ganz-thermodilution catheter at rest and during supine ergometer exercise before and after 5 mg intravenous Propranolol (P) (10 pats.) respectively 10 mg of intravenous Metoprolol (9 pats.). During exercise, P caused a significantly higher increase in pulmonary capillary wedge pressure (PCP) (15.0 +/- 4.0 to 25.3 +/- 4.0 mm Hg), than M (10.9 +/- 4.8 to 17.4 +/- 5.5 mmHg) (p less than 0.025). There was a uniform reduction of the cardiac output (CO), after P and M. P caused a reduction of the CO by a decrease in heart rate and stroke volume, M through a significantly greater decrease in heart rate (p less than 0.0005), without a change in stroke volume (p less than 0.05). The changes in PCP and stroke volume give evidence of a more negative inotropic effect of P compared to M.
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PMID:[Hemodynamic changes in patients with arterial hypertension after beta-receptor blockade with propranolol and metoprolol (author's transl)]. 73 94

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


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