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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Present knowledge of the mechanisms regulating release of renin is reviewed with particular emphasis on neural factors. Evidence is given for a direct effect of renal innervation on beta adrenergic receptors in juxtaglomerular cells, and for the involvement of reflex release of renin in conditions such as tilting and acute salt depletion. Participation of neural and nonneural mechanisms of control is also shown to occur in other conditions, such as aortic constriction and hemorrhage. The view is held that neural sympathetic factors might explain some of the renin disturbances found in essential hypertension. First, in patients with high renin hypertension part of the hypertension is renin-dependent, and these pressor levels of renin seem to be neurally induced since they can commonly be suppressed by beta adrenoreceptor blocking agents. Second, the hypothesis is presented that patients with low renin hypertension, at least those who have no volume disturbance, have a blunted sympathetic control of renin release. Therefore a sufficiently precise test of sympathetic activity, and possibly of body fluid volumes, should be associated with renin profiles for a better understanding of the pathophysiology of arterial hypertension and as a better guide to therapeutic management. Indeed, most of the available antihypertensive drugs act on sympathetic activity, body fluid volume or renin, and this multifaceted profile would provide more rational guidelines for treatment.
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PMID:Control of renin release: a review of experimental evidence and clinical implications. 0 64

The changes in plasma renin activity (PRA) during short-term salt depletion (and peroral furosemide on the first day) and after bolus injection of propranolol were compared to the change during long-term treatment with diuretic and with propranolol in 19 patients with benign primary hypertension. A highly significant correlation was found between PRA on short-term and long-term salt depletion (r=0.02). A highly significant correlation was likewise found between initial PRA and decrement of PRA after bolus injection of or long-term treatment with propranolol. Only a weak inverse correlation was found between PRA reached during short-term salt depletion or long-term diuretic treatment and the fall in diastolic BP during long-term treatment (r=0.60). No significant correlation was found between decrease in PRA on propranolol (bolus/long-term) and diastolic BP reduction. It is concluded that the short-term PRA response to salt depletion and propranolol in the individual patient gives a good prediction of the PRA level on long-term diuretic or propranolol treatment, but is of no value in predicting the BP reduction during treatment.
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PMID:Acute and long-term salt depletion and beta-blockade: plasma renin activity response and its relation to blood pressure reduction in long-term treatment. 2 64

24 h urinary sodium excretion was used to monitor salt intake in 36 patients with essential hypertension to determine whether limitation of the antihypertensive action of thiazide diuretics could be explained by increased salt appetitie stimulated by salt depletion. Sodium excretion in these patients was similar before treatment to that observed in normotensive controls, and no change was observed during 2 years' treatment with bendrofluazide. However, plasma-renin rose progressively over the 2 years even in 5 of 8 patients whose renin was not stimulated initially by diuretics. Thus, there is no evidence that a voluntary increase in salt intake limits the efficacy of diuretic treatment; on the other hand, progressive stimulation of the renin-angiotensin system may be an important limiting factor to the antihypertensive action of diuretics. If so, the antihypertensive effect of dietary salt restriction may be similarly limited.
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PMID:Salt intake and diuretic treatment of hypertension. 8 56

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

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

The data presented establish that in early or mild essential hypertension there is a state of inappropriate hypermineralocorticoid activity represented by the sum of aldosterone and 18-hydroxy-11-deoxycorticosterone concentrations in the plasma. This disturbance, associated with a "normal" or excessive salt intake, would produce the arteriolar cationic changes in sodium, potassium, calcium, or magnesium leading to hypersensitivity or hyperresponsiveness of the arteriolar actomyosin to normal levels of circulating norepinephrine or angiotensin. The nature of the cationic changes in the arteriolar cells responsible for the increased tonicity of the arteriolar actomyosin, which is the fundamental cause of essential hypertension, remains to be elucidated.
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PMID:The role of the adrenal cortex in human essential hypertension: keynote address. 19 54

A salt-free diet is usually useless or dangerous in the elderly subject. It has at present only rare indications, such as after acute pulmonary oedema or congestive heart failure during initial treatment. In all other cases, it may be replaced by a reasonable diet; sodium intake remains permitted, but naturally one should not fall in the opposite extreme. As in younger subjects, and provided one takes into consideration the subjacent renal condition, properly prescribed diuretics have transformed the situation in the treatment of heart failure as in essential hypertension. Naturally the patient still requires regular clinical supervision and laboratory tests which may in practice be limited to periodical estimation of blood urea and serum potassium, less regularly, blood sugar and uric acid.
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PMID:[Salt-free diet and diuretics in the elderly (author's transl)]. 21 98

One hundred fourteen hypertensives and 20 normal controls were examined using a new clinical technique of measuring 24-h urinary free 18-hydroxy-11-desoxycorticosterone (18-OH-DOC) excretion in response to dietary salt manipulations and ACTH injections. The object was to avoid potential errors of random plasma sampling. Mean urinary free 18-OH-DOC in normals on 110 milliequivalent sodium diet was 1.84 +/- 0.69 microgram (mean +/- SD) and represented about 2% of the daily secretion rate of this steroid. Both in normals and hypertensives, urinary free 18-OH-DOC approximately doubled on low salt (P less than 0.01 for each) and rose about 10 times in response to ACTH injection (P less than 0.05 and P less than 0.01, respectively). Plasma and urinary free 18-OH-DOC showed good correlation in patients with essential hypertension on a low salt diet (r = 0.45, P less than 0.01). Suppressed renin patients showed no propensity toward excess 18-OH-DOC excretion and hypertensives with elevated 18-OH-DOC could not be distinguished by their aldosterone levels, cortisol levels, nor their responses to various stimuli. These data suggest 18-OH-DOC is predominantly secreted under ACTH control and, to a smaller extent, in response to salt changes. Hypertension characterized by chronic overproduction of 18-OH-DOC forms only a small percentage of the hypertensive population. It is proposed that measuring 24-h urinary free 18-OH-DOC excretion may be the best method of assessing its rate of secretion without resorting to injection of radiolabeled material.
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PMID:Urinary free 18-hydroxy-11-desoxycorticosterone excretion in normal and hypertensive patients. 23 84

Information defining the renin-angiotension-aldosterone axis as a control system concurrently regulating salt balance and blood pressure has been applied to reexamine the role of renin in experimental and clinical forms of renovascular and renal hypertension, and thence to develop criteria for differentiating these entities. Experimentally, there are two models of renovascular hypertension; one is characterized by excess renin with reduced sodium (vasoconstrictor form) and the other by excess sodium with reduced renin (volume form). But with sodium depletion, the volume form converts to a vasoconstrictor form illustrating how the two factors coordinate to maintain blood pressure. In man, renovascular and renal hypertensions appear to be sustained by the same two mechanisms. Studies in man show that, in the absence of unilateral disease, the supine renal venous renin level in each kidney is consistently 24 percent higher than the peripheral level. Because of this constant relationship, the peripheral renin level is a measure of the renal secretion rate. Our studies indicate the curable unilateral renovascular hypertension is, in fact, renin-dependent vasoconstrictor hypertension. Three criteria, derived from four renin measurements, identify this situation: (1) Hypersecretion of renin is reflected by a high peripheral level when indexed against sodium excretion. (2) Lateralization of renin secretion with contralateral suppression rules out occult bilateral disease. It is indicated by V-A equal 0 from the uninvolved kidney. (3) (V-A)/A greater than 48 per cent from the ipsilateral kidney supports unilateralization. With data derived from patients with essential hypertension as a reference, the degree to which (V-A)/A is greater than 0.48 can be used to estimate the degree of renal ischemia, using Fick's principle. Corroborative evidence to support these three criteria can be developed from the blood pressure response to angiotensin blocking drugs or to antirenin therapy with propranolol. Clinical analysis validates these criteria to identify curable hypertension from unilateral renovascular or parenchymal disease. In patients with either occult or overt bilateral renal disease, the volume factor often predominates and is expressed by some suppression of plasma renin levels. Continued
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PMID:The renin axis and vasoconstriction volume analysis for understanding and treating renovascular and renal hypertension. 23 77

1. Urinary kallikrein was measured in 67 patients with essential hypertension and 25 normotensive subjects variously on unrestricted and low sodium diet. Also, the effect of orally applied hog pancreatic kallikrein on elevated blood pressure and kallikrein excretion was evaluated. 2. Urinary kallikrein was reduced in a large subgroup of patients with sustained essential hypertension. 3. With salt restriction, urinary kallikrein rose markedly in normotensive subjects and patients with borderline hypertension but not in those with sustained hypertension. 4. Oral kallikrein normalized reduced kallikrein excretion and lowered elevated blood pressure. 5. The rise in urinary kallikrein with oral kallikrein was due to an increased formation of endogenous enzyme. 6. A defective kallikrein-kinin system may be involved in both the low urinary kallikrein excretion and the hypertension.
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PMID:Low urinary kallikrein excretion and elevated blood pressure normalized by orally kallikrein in essential hypertension. 26 17


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