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

A father and son are described with a condition characterized by benign hypertension, potassium deficiency, increased aldosterone secretion rate (ASR), raised plasma volume and suppressed plasma renin activity (PRA). There were intermittent elevations of urine 17-ketosteroids and 17-hydroxycorticoids (17-OHCS) but no increase in urine THS, normal circadian rhythm of plasma 17-OHCS, and normal urine 17-OHCS response to dexamethasone and intravenous ACTH. Plasma ACTH and corticosterone secretion were not elevated. Pregnanetriol excretion was normal but urine pregnanediol was increased. At operation on the father no adrenal tumour was found; the excised left adrenal weighed 7 g. and showed nodular cortical hyperplasia; juxtaglomerular cells showed only occasional granules. Following operation hypertension persisted and ASR was half the preoperative value. All abnormalities in father and son were relieved by dexamethasone (DM) 2 mg. daily. The condition recurred following cessation of DM but was relieved by a second course of treatment. No such response to DM was seen in a normal subject or in a patient with Conn's syndrome. For a number of reasons it is suggested that patients with hypertension, increased ASR and low PRA be given a trial of dexamethasone treatment before undergoing adrenal surgery.
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PMID:Hypertension, increased aldosterone secretion and low plasma renin activity relieved by dexamethasone. 428 76

Adrenal-enucleated, mononephrectomized rats given a high salt diet rapidly develop malignant hypertension, characterized by the presence of necrotizing vascular lesions in a number of organs and tissues. If a normal salt intake is provided, or if hydrochlorothiazide is given together with a high salt diet, there is, instead, the delayed onset of benign hypertension which either stabilizes or increases in intensity extremely slowly; Such animals display few, if any, pathologic vascular changes other than occasional focal glomerular hyalinization, show insignificant cardiac enlargement, and do not exhibit alterations in the serum sodium or potassium. Occasional animals behave atypically and develop malignant hypertension despite normal salt consumption, demonstrating that in susceptible rats excess salt is not essential to this disorder. Hydrochlorothiazide given to rats that imbibed distilled water postoperatively prevented hypertension entirely for 97 days, when one of eight rats developed mild hypertension and some others reached what is regarded as a prehypertensive range. It is concluded that adrenal regeneration provides a physiological milieu favorable to the development of benign hypertension, which is not, as a rule, manifest until regeneration is complete. Salt excess converts the response into one in which malignant hypertension begins during regeneration and worsens rapidly thereafter until death. The course and findings are compared with those of the benign and malignant phases of clinical essential hypertension, and the implications of the similarities are discussed.
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PMID:Benign and malignant hypertension after adrenal enucleation in the rat. Relationship to salt intake, response to hydrochlorothiazide, and similarity to essential hypertension. 602 46

The hemodynamic mechanism of blood pressure response to angiotensin blockade is well established in "benign" but not in human malignant hypertension. We studied the changes in mean arterial pressure (MAP), cardiac index (CI), pulmonary wedge pressure (PWP), and in plasma volume (PV) induced by a single oral dose of captopril (150 mg) in 11 patients with malignant hypertension. Two hours after captopril, MAP fell from 178.5 +/- 5.8 to 151.8 +/- 7.8 mm Hg (p less than 0.001) (means +/- SEM) due to a fall in total peripheral resistance (TPR) (from 54.8 +/- 6.8 to 46.4 +/- 1.6 arbitrary units, p less than 0.001). However, there was a simultaneous increase in CI (from 3.29 +/- 0.13 to 3.70 +/- 0.15 liter/min/m2, p less than 0.001), and a decrease in PWP (from 15.3 +/- 3.5 to 11.0 +/- 2.5 mm Hg, p less than 0.001), while PV remained unchanged (from 4.02 +/- 0.26 to 4.12 +/- 0.12 liters, n.s.). Our data show that, in human malignant hypertension, blood pressure response to captopril is due to a decrease in TPR, but in contrast to benign hypertension, there is also a simultaneous increase in CI. Our results suggest that, in malignant hypertension, potentially high CI levels are artificially normalized by the increased TPR and may be fully disclosed by vasodilation.
Hypertension
PMID:Hemodynamic mechanism of blood pressure response to captopril in human malignant hypertension. 633 61

The purpose of the present study was to develop a controllable experimental model in the dog that would consistently and predictably produce a malignant hypertensive crisis, and to determine the sequential changes in renal function, salt and water balance, and hormones that are involved in the transition from benign to accelerated hypertension. Norepinephrine (NE) was infused continuously into the renal artery of unilaterally nephrectomized dogs that were maintained on 50 mEq sodium/day. The infusion rate of NE was increased each day according to the following schedule: 0.05, 0.1, 0.2, 0.3, 0.4, and 0.5 microgram/kg/min. During the first 4 to 5 days of intrarenal NE infusion, there was a progressive decrease in glomerular filtration rate (GFR) and effective renal plasma flow (ERPF), and increases in plasma renin activity (PRA), mean arterial pressure (MAP), and filtration fraction. At the end of this period of benign hypertension, MAP had risen from a control value of 91 +/- 4 to 132 +/- 8 mm Hg, in association with approximately a 10-fold increase in PRA and a 40% reduction in renal function. Then, suddenly, during the subsequent 24-hour infusion period, the MAP increased abruptly in all animals (MAP = 156 +/- 8 mm Hg), and a hypertensive crisis occurred. This crisis was associated with the following: salt and water depletion, hyponatremia, hypovolemia and hemoconcentration, polydipsia, marked activation of the renin-angiotensin-aldosterone system, increased plasma cortisol concentration, hemolysis, marked impairment in renal function, lethargy, and vomiting.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension
PMID:Malignant hypertensive crisis induced by chronic intrarenal norepinephrine infusion. 637 96

Computerised apex- and echocardiography was used to study left ventricular dimensions and function in 13 patients with untreated malignant hypertension and eight with severe benign hypertension. All patients had normal left ventricular cavity dimensions. Five benign hypertensives and malignant hypertensives with a previous history of hypertension had significant thickening of the septum and posterior wall. In eight malignant hypertensives without a previous history wall thicknesses were normal. The absence of ventricular hypertrophy in some cases of malignant hypertension suggests that it is sometimes of rapid onset and not preceded by a non-malignant phase. although fractional shortening and peak Vcf were normal in all the hypertensives, diastolic left ventricular function was frequently abnormal with delayed mitral valve opening, reduced peak rate of filling, and outward endocardial motion during isovolumic relaxation. Malignant hypertensives showed a cavity shape change during isovolumic contraction, and in those without a previous history the aortic second heart sound occurred earlier. The abnormalities of function are probably the result of a combination of factors including pressure overload, abnormal myocardial properties, and myocardial ischaemia, either regional or generalized and secondary to arteriolitis.
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PMID:Echocardiographic features of malignant hypertension. 645 15

Comparative morphometric study of the juxtaglomerular complex and interstitial cells of the corticomedullary zone of the kidney was performed on the autopsy material in benign (26 cases) and malignant hypertension; for control, 15 cases were examined. The state of intrarenal arteries, arterioles and the degree of medulla interstitium sclerosis were taken into consideration. No activation of the renin-producing system was observed morphometrically in "benign" hypertension while it was pronounced in malignant hypertension. The hypothesis is put forward on the reserve renin secretion by mesangial cells in malignant hypertension. It is assumed that the prostaglandine-synthesizing function of the interstitial cells is not damaged in benign hypertension, but it is significantly lower in malignant course of the disease. Relationship is shown between the alterations of intrarenal arteries and arterioles and the degree of the medulla sclerosis in malignant hypertension.
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PMID:[Endocrine structures of the kidney in hypertension]. 650 76

The water and sodium content of the saphenous vein was measured in 26 dogs with one-kidney, one wrapped hypertension. For comparison, the same measurements were performed on the contralateral saphenous vein which was removed prior to the induction of hypertension. Malignant hypertension characterized by blindness and a rise in plasma renin activity, developed in 10 dogs. The course of hypertension in the remaining 16 dogs was benign. In benign hypertension, the water and sodium content of the saphenous vein was increased. In contrast, the water content of the saphenous vein was unchanged and its sodium content fell in dogs with malignant hypertension. The dogs with malignant hypertension had a greater sodium content of the saphenous vein prior to the induction of hypertension than the dogs with benign hypertension. The findings indicate that the loss of body water and sodium that has been described in malignant hypertension also affects the composition of blood vessels. The sodium content of blood vessels may be a predictor of the dog's response to a hypertension-producing stimulus.
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PMID:Abnormalities of vascular wall sodium content in dogs with benign and malignant renal hypertension. 672 84

Only 1 of 7 dogs with long-standing renovascular hypertension showed clear changes in the fundus. No distinct retinopathy was seen in the others. Ophthalmoscopy alone is thus of limited value in assessing the progress of benign hypertension in the dog.
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PMID:Examination of the fundus of the eye of renal hypertensive dogs. 672 7

Although blood pressure standards in aircrew members have been revised periodically over the past 70 years, hypertension still remains one of the most controversial problems in aviation medicine. Improved clinical knowledge and operational experience vindicate a more liberal attitude for acceptable blood pressure levels. Applicants for flying training presenting labile hypertension may be accepted. Also, experienced, older aircrew with benign hypertension controlled by drugs without adverse reactions and without target organ disease may remain on flying status. In order to avoid compromising flight safety, long-term monitoring of flight crew for the diagnosis of hypertension together with the evaluation of anti-hypertensive drugs in aircrew is urgently required.
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PMID:Hypertension and orthostatic hypotension in applicants for flying training and aircrew. 683 May 61

Renal vascular changes in severe hypertension were studied. Twenty-five cases selected from 4,629 autopsies were classified into 2 groups according to the cause of death: group 1 (9 cases died of renal failure) and group 2 (16 cases of extra-renal death). Group 1 had been clinically diagnosed as malignant hypertension and had the hallmarks of malignant nephrosclerosis characterized by arteriolar fibrinoid necrosis and edematous intimal thickening. Group 2 had been clinically diagnosed as benign hypertension and basically exhibited the changes of benign nephrosclerosis. However, about half of the cases of group 2 had arteriolar fibrinoid necrosis, though the lesion was usually less extensive than in group 1. Immunofluorescence revealed similar deposits of immunoglobulins and fibrinogen in the site of fibrinoid necrosis observed in both groups. As for the changes of interlobular arteries, a quantitative analysis disclosed a distinctive difference between groups 1 and 2 with respect to the narrowing ratio of arterial lumina, though edematous intimal thickening was recognized on relatively rare occasions in the distal interlobular arteries in a few cases of group 2. From the results, the problem of transition from the benign to malignant nephrosclerosis was discussed.
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PMID:Renal vascular lesions in severe hypertension. Transitional changes from benign to malignant nephrosclerosis. 686 4


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