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

1. Restriction of dietary salt intake does not affect the development or maintenance of hypertension in rats with unilateral renal ischaemia whether the contralateral kidney is present (Goldblatt 2 model) or not (Goldblatt 1 model). 2. Acute dietary salt depletion induces a similar loss of sodium and fall in body weight with little change in blood pressure in both normal and hypertensive rats. 3. Excision of the ischaemic kidney in rats with short-term (less than 50 days) Goldblatt 2 hypertension restores the mean blood pressure to normal, whereas Goldblatt 1 hypertensive rats show only a partial response. Previous salt depletion of this model enhances the blood pressure response to nephrectomy. 4. Sodium retention plays no part in the development or maintenance of Goldblatt 2 kidney hypertension. However, although sodium retention is normally involved in the Goldblatt 1 model, hypertension can develop in the absence of dietary sodium.
Clin Sci Mol Med 1976 Sep
PMID:Influence of sodium restriction upon two models of renal hypertension. 96 57

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.
Clin Sci Mol Med Suppl 1975 Jun
PMID:Hypotensive and renin-suppressing activities of propranolol in hypertensive patients. 105 79

1. The metabolic role of arterial angiotensin I-forming enzyme (i.e. renin activity) was studied in total homogenates and in subcellular fractions of the aorta of normotensive and hypertensive rats. 2. Angiotensin I-forming enzyme was measured in (a) uninephrectomized rats rendered hypertensive with D-aldosterone and sodium chloride (10 g/l drinking solution, (b) rats treated in the same manner but with the addition of spironolactone, and (c) control rats. 3. Hypertension developed in aldosterone-treated rats within 3-6 weeks and was associated with decreased plasma and renal renin values. Total aortic renin activity was up to sixfold higher in the hypertensive animals than in control animals and there was an increased ratio of supernatant to microsomal renin activity in the aorta. 4. In spironolactone-treated rats blood pressure and total aortic renin concentrations were comparable with those in the control rats. 5. The results support the hypothesis that renin generated at local vascular sites, which is independent of circulating renin levels, contributes to regulation of blood pressure.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Effects of aldosterone and spironolactone on arterial renin in rats. 107 85

1. Infusion of angiotensin II antagonist failed to restore the blood pressure of short-term Goldblatt 2-kidney hypertensive rats to normal levels before and after sodium restriction. 2. The blood pressure of both normal and sodium-restricted Goldblatt 2 hypertensive rats remained elevated 6 h after bilateral nephrectomy. 3. The residual hypertension found during antagonist infusion and after bilateral nephrectomy is not maintained by the renin-angiotensin system or sodium retention.
Clin Sci Mol Med Suppl 1976 Dec
PMID:The role of sodium retention in Goldblatt 2-kidney hypertension in the rat. 107 86

1. Sodium-deficient diet failed to alter development and maintenance of severe renal hypertension produced in the rat by ligation of the aorta between the renal arteries. 2. High sodium diet did not alter the early phase of this hypertension, but significantly decreased blood pressure elevation in the late phases. 3. The decrease in blood pressure produced by high sodium intake does not appear to be mediated by renin suppression. 4. Frusemide effectively reduced blood pressure and renin at all phases.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Salt, frusemide and renin in severe experimental renal hypertension. 107 87

1. The casual blood pressure is the sum of the relatively stable basal pressure taken under defined conditions of rest and the labile supplemental pressure (casual minus basal), which represents the response to the current degree of physical, mental and probably metabolic stimulation. 2. The basal and supplemental blood pressures behave differently and it seems likely that different factors are involved in their pathogenesis. 3. The 5 and 8 years follow-up mortality is closely related to the basal pressure but not to the supplemental pressure. 4. The rise with age in the basal blood pressure is greater in the relatives of substantial hypertensive patients than in population control subjects. 5. Above the age group 30-39 years there is an increase in the rate of rise of the mean basal blood pressure with age among the first-degree relatives of hypertensive patients. In a population control group an acceleration in the rate of rise of the mean basal blood pressure with age also occurs but a decade or more later than in the relatives of hypertensive patients. 6. In males the mean supplemental pressures (systolic and diastolic) do not rise appreciably with age and the mean supplemental pressures of first-degree relatives and control subjects do not differ appreciably. 7. In females the mean supplemental pressures rise with age but, except after age 60 years, the pressure rise in first-degree relatives is only a little greater than in control subjects. 8. When hypertensive patients with similar casual blood pressures are compared the basal blood pressures are higher in patients with glomerulonephritis than in essential hypertensive patients. 9. In the first-degree relatives of substantial hypertensive patients high-ranking basal blood pressures occur much more frequently than in general population control subjects. 10. The close resemblance of the blood pressures in like twins indicates that genetic or familial factors have an important influence on blood pressure, and on the occurrence of frank hypertension.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Casual, basal and supplemental blood pressures in 519 first-degree relatives of substantial hypertensive patients and in 350 population controls. 107 88

1. Total exchangeable sodium was measured in rats by a radio-sodium equilibration method, before and after the production of hypertension by clipping the left renal artery, with or without contralateral naphrectomy. 2. Clipping of one renal artery with removal of the other kidney produced severe hypertension with no significant changes in exchangeable sodium or plasma renin levels. 3. Clipping of one renal artery without contralateral nephrectomy produced severe hypertension in some animals, but little change in blood pressure in others. The animals which developed severe hypertension had a marked increase in exchangeable sodium with a concomitant rise in plasma renin; the animals with smaller rises in blood pressure did not have these changes. 4. The fact that both plasma renin levels and exchangeable sodium levels increase according to this method, suggests that hypertension in the two-kidney model is renin-dependent.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Exchangeable sodium in experimental hypertension in rats. 107 89

1. The haemodynamic changes during the development of hypertension in rabbits have been studied for 1 week before and 4-5 weeks after sham-operation (thirteen rabbits) or bilateral renal cellophan wrapping (thirteen rabbits), Doppler flowmeters being used to measure cardiac output. 2. There was a significant but transient rise in cardiac output on post-operative day 4 in six of thirteen sham-operated rabbits and six of thirteen renal-wrap rabbits before development of hypertension. Both groups showed the same rise in mean cardiac output of 10%. The reise in cardiac output was more transient than in other species, and was not essential for subsequent development of hypertension.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Cardiac output changes during experimental renal hypertension in the rabbit. 107 90

1. In renal hypertensive dogs, the slope of the relation between either stroke volume or cardiac output and end-diastolic pressure is shifted to the right of the normal curves. 2. The maximum to which stroke volume or cardiac output can be raised during loading is significantly less. These changes in cardiac performance appear to be unrelated to the severity of hypertension.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Ventricular performance after onset of renal hypertension. 107 91

1. Bilateral compression of adrenal glands combined with unilateral nephrectomy and followed by imposition of a high sodium chloride intake caused severe hypertension in all rats, accompanied by enlargement of the heart, kidneys and adrenal glands, atrophy of the thymus and severe nephrosclerosis. 2. Digitoxin treatment delayed the onset, reduced the incidence and ameliorated the magnitude of the hypertensive response in such rats; it also reduced the degree of cardiac hypertrophy, the severity of nephrosclerosis and completely prevented enlargement of the adrenals and kidneys or atrophy of the thymus.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Delayed onset and reduced severity of adrenal-compression hypertension in rats treated with digitoxin. 107 96


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