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

31 patients with a diastolic blood-pressure between 95 and 109 mm Hg have been treated for two years with a regimen involving a moderate restriction of salt in the diet. The results are compared with those in a control group and in a drug-treated group. Salt restriction has reduced the diastolic blood-pressure by 7.3+/-1.6 mm Hg, a result similar to that in patients treated with antihypertensive drugs. In the untreated group the diastolic blood-pressure rose by 1.8+/-1.1 mm Hg. Most patients did not achieve the desired amount of salt restriction and a stricter adherence to the diet might have caused further falls in blood-pressure. Excessive salt intake is probably a major cause of the epidemic of hypertension in "civilised" countries and a reduction in salt intake may help to control the epidemic. In persons with a diastolic blood-pressure between 90 and 105 mm Hg salt restriction should be tried before drugs.
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PMID:Hypertension treated by salt restriction. 7 60

In the course of the development of desoxycorticosterone-acetate-salt hypertension the animals were noted to display high appetite of sodium chloride, a considerable increase of the weight of the heart, kidneys and adrenal glands, of the diameter of the glomeruli and the surface of the cortical and medullar zones of the kidneys, a decrease of the sodium and potassium gradient in the renal tissue. Adaptation to hypoxy is noted so cause a decrease in the interventricular factor, in the width of the glomerular zone of the adrenal glands, in the sodium concentration in the erythrocytes, an increase in the mass of the medullar layer of the kidneys, and an increase in the sodium and potassium gradients. When adaptation to hypoxy is combined with the effect of desoxycorticosterone-acetate-salt, hypertension develops to a lower degree than in non-adapted animals.
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PMID:[Certain changes in the water-electrolyte metabolism in desoxycorticosterone acetate salt hypertension in rats adapted to high altitude hypoxia]. 12 78

Swimming, if undertaken for 1 hr/day, 3 days/week for 6 weeks prior to treatment with DOCA, unilateral nephrectomy, and salt-loading, delayed the development of hypertension in rats. If the swimming were undertaken concurrently with or after initiation of treatment with the above hypertensive regime, then it was without effect on the level of blood pressure attained or the length of time required to attain a given blood pressure. Swimming in itself resulted in a significant increase in arterial blood pressure. Previous training, such as swimming, may delay the development of hypertension through an alteration in vascular structure or smooth muscle sensitivity. The increase in blood pressure noted in physically trained rats may be a consequence of the training regime itself acting as a stressor.
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PMID:Relationships between physical training and DOCA hypertension in rats. 13 Jun 37

Clinical, experimental and pathologic studies strongly indicate that hypertension is a major factor in coronary heart disease, sudden death, stroke congestive heart failure and renal insufficiency. The deleterious effect of the elevated blood pressure on the cardiovascular system appears to be due mainly to the mechanical stress placed on the heart and blood vessels. Humoral factors and vasoactive hormones such as angiotensin, catecholamines and prostaglandins may play a role in the pathogenesis of hypertensive cardiovascular disease but this role has not yet been defined and is probably secondary. Hypertension and the resulting increase in tangential tension on the myocardial and arterial walls, leads to the development of hypertensive heart disease and congestive heart failure as well as hypertensive vascular disease that affects not only the kidneys but also the heart and brain. Hypertensive vascular disease involves both large and small arteries as well as arterioles and is characterized by fibromuscular thickening of the intima and media with luminal narrowing of the small arteries and arterioles. The physical stress of hypertension on the arterial wall also results in the aggravation and acceleration of atherosclerosis, particularly of the coronary and cerebral vessels. Moreover, hypertension appears to increase the susceptibility of the small and large arteries to atherosclerosis. Thus the patient with hypertension is a candidate for both hypertensive and atherosclerotic vascular disease of the coronary and cerebral vessels leading to occlusive disease of both the large and small arteries and resulting in myocardial infarction and stroke. Other major complications of hypertensive vascular disease include rupture and thrombotic occlusion of blood vessels, especially in the brain. Disease of the arterial media, which begins in childhood with the deposition of calcium in the vessels, may be an important cause of arterial hypertension. This form of hypertension may manifest itself in adults as arteriosclerotic hypertension and lead to cardiovascular complications very similar to those of essential hypertension. The relation of arteriosclerotic hypertension to nutritional factors, including dietary salt intake, deserves study.
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PMID:Role of hypertension in atherosclerosis and cardiovascular disease. 13 91

Hypertensive Goldblatt-rats have higher than normal Na-appetite and an enhanced Na-output. They have normal plasma Na- and K-concentration and kidney weight but a significantly reduced plasma volume. The amount of renal membrane protein and the renal Na-K-ATPase-activity of hypertensive rats was found to be significantly below that of controls. In order to evaluate the role of Na-appetite, Na-excretion rate and renal Na-K-ATPase-activity in the electrolyte balance, Goldblatt-rats with a stable hypertension and control animals were put for 8 days on a Na-free diet. Na-excretion rate of control rats reached a minimum (13 muEq/100 g x 24 hr) within 5 days and was maintained on this level up to the end of the experiment. Na-free diet did not alter either the kidney weight or the amount of membrane protein of the animals. However, in salt-free fed control rats total renal Na-K-ATPase-activity was found elevated by about 10% as compared to animals maintained on normal diet. Goldblatt-rats continuously excreted significantly higher amounts of Na (35 muEq/100 g x 24 hr), had sharply reduced plasma volume and plasma Na- concentration. The renal Na-K-ATPase-activity should no adaptation in gold blatt-rats. In all animals studied the rate of Na-excretion showed a close indirect correlation with the renal Na-K-ATPase-activity. It is concluded, that Goldblatt-rats depend on dietary Na to a higher extent than controls because of their reduced capacity to retain Na. The increased Na-appetite of hypertensive rats is a factor secondary to Na-loss.
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PMID:Interdependence of Na-excretion, plasma electrolytes, plasma volume and renal Na-K-ATPase-activity in hypertensive rats. 13 99

The urinary excretion of 3beta,16beta-dihydroxy-5-androsten-17-one (16beta-OH-DHEA) is increased in patients with low renin essential hypertension. This steroid and its isomer 3beta,17beta-dihydroxy-5-androsten-16-one (16-oxo-A) have also been reported to have mineralocorticoid activity in adrenalectomized rats. These findings have led to the postulate that excessive secretion of 16beta-OH-DHEA may be responsible for the production of low renin essential hypertension. In this study unilaterally nephrectomized salt loaded rats injected once a week with 30 mg of 11-desoxycorticosterone acetate per/kg of body weight for 2 month periods developed hypertension. Rats given similar amounts of 16beta-OH-DHEA or 16-oxo-A and rats given no steroids did not develop hypertension. We conclude that it is unlikely that 16beta-OH-DHEA and 16-oxo-A are direct causative factors in the production of low renin essential hypertension.
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PMID:Blood pressure changes following chronic administration to rats of 3beta,16beta-dihydroxy-5-androsten-17-one, 3beta,17beta-dihydroxy-5-androsten-16-one and 21-hydroxy-4-pregnene-3,20-dione-21-acetate. 13 80

Young and adult uninephrectomized male rats (aged 25 and 87 days respectively) were exposed to an increased salt intake (1% saline as the only drinking fluid) either alone or in combination with DOCA-treatment for 25 and 46 days respectively. Age dependent differences of interrelationships between saline intake (SI), blood pressure (BP) and kidney weight (KW) were studied during development of salt and DOCA-salt hypertension to specify possible factors involved in the higher susceptibility of the young rats to these regimes. Correlation analysis was employed using the step-wise regression procedure. Only in the young rats did saline treatment induce an increase in KW, which preceded the development of mild hypertension. This age group also responded to DOCA-saline treatment with a more pronounced increase in both BP and KW. SI was higher in the young than adult rats exposed to either saline or DOCA-saline treatment. This, however, does not account by itself for the higher hypertensive response of the young rats, since there was no primary relationship between SI and BP in the hypertensive groups. Increase in KW accompanying development of hypertension was dependent on BP in the young rats and on SI in adult rats. This indicates that saline and DOCA-saline treatment renders the kidneys of young rats more sensitive to damaging effects of BP, which play a part in the more pronounced hypertensive response.
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PMID:Age differences in interrelationships between saline consumption, blood pressure and kidney weight in salt hypertension in the rat. 14 81

Dahl hypertension-resistant (R) and hypertension-sensitive (S) rats were used to determine whether cadmium-induced hypertension is dependent on genetic predisposition. In experiment I, 16 wk-old R and S rats of both sexes were injected with two doses of cadmium (1 and 2 mg/kg body wt, ip), whereas the controls received the same volumes of saline. Hypertension and renal vascular changes were observed in cadmium-injected S rats but not in R rats. The S females appeared more sensitive than S males to the hypertensinogenic effect of cadmium. In experiment II, groups of weanling female R and S rats were given 0, 1, 2.5, 5, or 10 mg cadmium/liter drinking water and fed either a low-salt (0.4% NaCl) or a high-salt (4% NaCl) diet for 28 wk. Cadmium produced cardiac hypertrophy (1 mg cadmium/liter) and hypertension associated with renal vascular changes (1--5 mg cadmium/ liter), and it enhanced proteinuria (1-10 mg cadmium/liter) in S rats on a low-salt diet. Also, the development of salt-induced hypertension was accelerated in cadmium-fed (1 and 2.5 mg/liter) S rats. These adverse effects of cadmium were not detected in R rats on either salt diet. In experiments I and II, cadmium concentrations in the kidneys and liver of S rats were higher (P less than 0.001) than in those of R rats. These data indicate that genetic differences influence the pathogenesis of cadmium-induced hypertension.
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PMID:Genetic influence on cadmium-induced hypertension. 15 9

The role of the renin--angiotensin system in the regulation of blood pressure in dogs and in human subjects was assessed by the use of the nonapeptide converting enzyme inhibitor (CEI), permitting the following conclusions: 1) In the normal, sodium replete dog, the renin--angiotensin system plays little role in the regulation of blood pressure. 2) As sodium depletion progresses, the renin--angiotensin system becomes increasingly important in the maintenance of blood pressure. In the markedly hypovolemic animal, blocking the conversion of angiotensin I to angiotensin II leads to prolonged hypotension of shock-like levels. 3) The renin--angiotensin system is responsible for the initiation of renovascular hypertension. Blood pressure does not rise during chronic renal artery constriction when the generation of angiotensin II is prevented by the CEI. Although angiotensin II is essential for the initiation of the elevated blood pressure, the renin--angiotensin system plays a decreasing role in the maintenance of the chronic hypertension as sodium and water are retained, and plasma volume increases. 4) In congestive failure induced in the conscious dog by circulatory impairment, the renin--angiotensin--aldosterone system plays an essential role in the compensatory response. During chronic administration of the CEI, the animal cannot compensate even for a relatively mild degree of constriction, and remains hypotensive. In the dog with congestive failure, as in the dog with renovascular hypertension, plasma renin activity (PRA) and plasma aldosterone are elevated early in the syndrome; during this phase, injection of the nonapeptide produces a marked drop in blood pressure. With the retention of sodium and water, and expansion of plasma and extravascular fluid volumes, PRA and plasma aldosterone return to control levels in the new steady state. The inhibitor no longer produces a drop in blood pressure. Thus, the sequential changes in the renin--angiotensin--aldosterone system are remarkably similar in renovascular hypertension and congestive failure. 5) In the normal, salt replete human subject the renin--angiotensin system plays little role in the regulation of blood pressure either in the recumbent or upright posture. However, with relatively mild sodium depletion, the CEI transiently lowers blood pressure even in the recumbent subject. In the absence of angiotensin II such sodium-depleted subjects are unable to compensate when tilted upright, and faint within minutes.
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PMID:Renin--angiotensin antagonists and the regulation of blood pressure. 18 95

1. Acute severe sodium subtraction (20-25% of total exchangeable sodium) before or during treatment with adrenocorticotrophic hormone (ACTH) does little to modify the increase in blood pressure induced by ACTH. 2. Chronic low salt diet, less than 5 mmol/day, abolishes the blood pressure increase, but the response can be restored by increasing the sodium intake to as little as 10 mmol/day. 3. 17alpha,20alpha-Dihydroxyprogesterone infused concurrently with other adrenal steroids will mimic ACTH hypertension and perhaps represents a new class of steroid capable of influencing blood pressure.
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PMID:Further unravelling of the causes of ACTH-induced hypertension in the sheep. 19 14


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