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

Arteriography in two patients with renovascular hypertension suggested fibromuscular hyperplasia, mainly affecting the right renal artery. When saralasin was infused intravenously there was no fall in blood-pressure in either patient. However, both had a raised renal-vein plasma-renin activity on the affected side, relative to the unaffected kidney. Auto-transplantation resulted in a sustained reduction in arterial pressure in both patients. A negative saralasin test should not necessarily exclude further investigation of young patients with severe hypertension.
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PMID:Failure of saralasin to predict a response to surgery in renovascular hypertension. 6 20

This study deals with the histochemical specificity of crystal violet staining. Histological dyes such as crystal violet (CI 42555), ethyl violet (CI 42600) and methyl violet (CI 42535) are regularly employed for the assessment of juxtaglomerular granulation (WILSON 1952; FRIEDBERG and REID 1966; MARIUZZI and NENCI 1966). WILSON's modification of BOWIE's procedure is the staining method most frequently used for demonstration of 'renin granules' in the juxtaglomerular cells (JC). It has been assumed that JC granularity parallels renin-induced hypertension (PITTS 1968).
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PMID:Non-specificity of crystal violet staining for renin granules. 7 Sep 39

The concept of the "inappropriate" has a well-defined and easily comprehended meaning when applied to tumour secretion of antidiuretic hormone (A.D.H., vasopressin). When applied to high A.D.H. in other situations such as nephrotic syndrome, congestive cardiac failure, or cirrhosis, the use of the term "inappropriate secretion" simply reflects the fact that an easily measured controlling factor (plasma tonicity) is being overridden by a less easily measured one (effective extracellular volume). Similarly, sodium excretion in hypertension is said to be inappropriately low for the raised renal perfusion pressure: in this case inappropriateness results from the antinatriuretic effect of a minor degree of sodium depletion produced by pressure natriuresis. A similar objection can be made to the application of the term to the relations between renin or angiotensin-II concentrations and blood-pressure in some forms of hypertension. Since inappropriateness merely reflects the position and predilections of the observer, the widespread use of the term should be abandoned.
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PMID:On the inappropriate in hypertension research. 7 8

Injection of saralasin or converting-enzyme inhibitor produced a small variable reduction of blood-pressure in rats with two-kidney hypertension. Prolonged infusion of the inhibitors gradually reduced blood-pressure to normal. Control infusions of saralasin in normal animals and of dextrose in normal and hypertensive animals did not reduce blood-pressure. Plasma-renin concentration correlated significantly with the early but not with the later fall of blood-pressure. Plasma-concentrations of renin and angiotensin II were closely related except in rats receiving converting-enzyme inhibitor, when angiotensin II was relatively reduced. The gradual reduction of arterial pressure by saralasin was not associated with increased urinary sodium excretion.
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PMID:Correction of renal hypertension in the rat by prolonged infusion of angiotensin inhibitors. 7 29

Pronounced hypoaldosteronism was found in three young women with hypertension and symptoms of mineralocorticoid overproduction--i.e., hyporeninaemia, hypokalaemia, and a fall in blood-pressure after diuretic therapy. Plasma 11-deoxycorticosterone and 18-hydroxy-11-dooxycorticosterone concentrations were normal Treatment with dexamethasone induced a return to normal of blood-pressure and plasma-potassium and an increase in plasma-renin activity and urinary aldosterone excretion. The data suggest that hypertension in these patients is maintained by overproduction of an unknown adrenocorticotropindependent mineralocortocoid.
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PMID:Dexamethasone-responsive hypertension in young women with suppressed renin and aldosterone. 7 49

The angiotensin-blocking agent, saralasin, was given by rapid intravenous (bolus) injection to 21 hypertensive patients. A marked depressor response (average blood-pressure decrease of 30 mm Hg systolic and 20 mm Hg diastolic at 10 minutes after injection) was noted in 13 patients, of whom 11 had renovascular hypertension and 2 had high-renin essential hypertension. No change from prebolus blood-pressure was apparent at 10 minutes in 8 control patients with essential hypertension and normal or low peripheral plasma-renin activity. In all patients, blood-pressure response to saralasin bolus (10 mg) correlated with blood-pressure response to subsequent infusion of saralasin (10 microgram/kg/min). Blood-pressure response to rapid intravenous injection of saralasin--the "saralasin bolus test"--has many characteristics of an ideal screening procedure for renin-mediated hypertension.
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PMID:Saralasin bolus test. Rapid screening procedure for renin-mediated hypertension. 7 52

Plasma-renin-activity (P.R.A.) was raised in 9 of 15 hypertensive children with pyelonephritic scarring secondary to urinary-tract infection and vesicoureteric reflux and also in 8 of 100 normotensive children with such scars. P.R.A. was much less likely to fall with age in normotensive children with renal scarring than in normal children. The identification of hyperreninaemic normotensive children with renal scarring is important, since P.R.A. may prove to be of value in early identification of children at risk of developing hypertension. A longitudinal follow-up is proposed to establish this hypothesis.
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PMID:Renin and blood-pressure in children with renal scarring and vesicoureteric reflux. 7 5

Captopril (SQ 14 225), an orally active inhibitor of angiotensin-converting enzyme, was given to 7 hypertensive patients with chronic renal failure whose plasma-creatinine ranged from 1.5--7.4 mg/dl; whose plasma-renin activity was normal; whose hypertension was not controlled by previous therapy consisting in 5 patients of three or more antihypertensive drugs; and whose blood-pressures averaged 176/111 +/- 11/3 mm Hg. Inhibition of converting enzyme by oral captopril, 200 mg twice daily, reduced blood-pressure to 156/100 +/- 9/5 mm Hg. 5 patients needed additional treatment by frusemide 40--250 mg/day orally. With this combined regimen the blood-pressure of all patients averaged 126/85 +/- 4/3 mm Hg after 8 +/- 2 weeks of captopril. The drug was well tolerated. These results suggest that inhibition of angiotensin-converting enzyme with or without sodium depletion is an efficient treatment for hypertension associated with chronic renal failure. It appears that although renin levels in patients with this condition may be "normal", they are inappropriate in relation to the subtle degree of sodium retention that occurs with this disorder.
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PMID:Innappropriate renin secretion unmasked by captopril (SQ 14 225) in hypertension of chronic renal failure. 8 Jun 34

The renal abnormality which causes hypertension in the Milan hypertensive strain of rats disappears as hypertension develops. Because of the many analogies between the condition in these rats and "essential" hypertension in man, the same pattern of change may occur if a renal abnormality is the cause of essential hypertension in man. This hypothesis was tested in two groups of young normotensive subjects matched for age, sex, and body-surface area; in the first group both parents were hypertensive, and in the second group both parents were normotensive. Renal plasma-flow, glomerular filtration-rate, plasma-volume, plasma-renin activity, plasma-concentrations of Na+, K+, and catecholamines, 24 h urinary excretion of Na+, K+, and aldosterone, and the cardiac index were measured so that renal function and the role of factors affecting blood-pressure regulation could be assessed. Renal plasma-flow was significantly higher (p less than 0.01) in the first group, whereas results of tests for all the other factors were almost the same in both groups. The hypothesis that a primary kidney abnormality causes hypertension in a proportion of patients with essential hypertension is proposed.
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PMID:A renal abnormality as a possible cause of "essential" hypertension. 8 3

Percutaneous transluminal renal angioplasty (P.T.R.A.) was performed in a 43-year-old woman with medial fibroplasia of the right main renal artery that was causing high-grade stenoses and severe hypertension. The procedure led to a virtually complete dilatation of the stenosing lesions and a prompt and lasting fall in blood-pressure to normal. Hypersecretion of renin from the right kidney was also promptly suppressed. The procedure was well tolerated by the patient and no complications were discerned. P.T.R.A. deserves further investigation to assess its role in the management of renovascular hypertension.
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PMID:Percutaneous transluminal angioplasty for severe renovascular hypertension due to renal-artery medial fibroplasia. 8 70


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