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

We investigated the role of arginine-vasopressin (AVP) in maintaining the blood pressure of spontaneously hypertensive (SH) rats (stroke-prone strain) with established hypertension (22--28 weeks of age). In comparison with normotensive Wistar Kyoto (WKY) rats, plasma AVP concentrations of SH rats with benign hypertension (BH) were elevated twofold and in rats with severe or malignant hypertension (S-MH), fourfold. The height of the blood pressure was quantitatively related to plasma AVP in both BH and S-MH rats, the overall correlation coefficient being 0.66 (p less than 0.001). The intravenous injection of a specific AVP antiserum into conscious and unrestrained rats lowered blood pressure in 4 BH rats by 48 +/- 14 mm Hg and in 4 S-MH rats by 78 +/- 10 mm Hg and had only a marginal effect in 4 normotensive WKY rats. Infusion of saralasin did not lower blood pressure in WKY and BH rats and reduced blood pressure in only 2 of 7 S-MH rats tetsted (by 15 and 20 mm Hg). During AVP infusion the blood pressure of SH rats increased more (p less than 0.001) and heart rate fell much less (p less than 0.001) than in WKY rats. It is concluded that in SH rats with established hypertension, plasma AVP plays an important role in the maintenance of high blood pressure, while the renin-angiotensin system plays a minor or no role.
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PMID:Studies on the role of vasopressin in blood pressure control of spontaneously hypertensive rats with established hypertension (SHR, stroke-prone strain). 9 26

Many children who suffered acute lead poisoning in Queensland eventually died with contracted kidneys. In most cases the kidneys were granular and showed microscopically fibrosis, hypertensive vascular changes and "alterative glomerulitis". Clinically in these patients, hypertension and chronic renal insufficiency had always preceded death which was usually due to uraemia. In a minority of cases the kidneys showed the changes of benign hypertension but were unusually small; fibrosis and "alterative glomerulitis" were not present. Clinically these patients had had hypertension but minimal renal insufficiency and death was usually due to cerebral haemorrhage. The evidence indicates that lead caused severe damage to the kidney at the time of the lead intoxication by some mechanism other than hypertension. The sequence of events postulated comprises severe renal damage with destruction of glomeruli during childhood lead poisoning, disappearance of the destroyed tissue during childhood and adolescence, onset of hypertension in adolescence or early adult life, gradual onset and progress of chronic uraemia during which fibrosis and granularity developed. In milder cases the sequence is not complete because renal function has remained adequate.
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PMID:The pathology and pathogenesis of chronic lead nephropathy occurring in Queensland. 36 88

The case of a 34-year-old woman who developed uremia secondary to renal thrombotic microangiopathy after taking oral contraceptives for 3 years is reported. The case is unusual in that the clinical manifestations of nephropathy and terminal kidney failure were preceded by an almost 1-year development with benign hypertension. During the final stage (3-4 weeks prior to complete development of uremia), hemolysis was observed only once and malignant hypertension not at all. The question, if and when reversible hypertension due to oral contraceptives becomes persistent renal hypertension, can be answered only after long-term observations with careful documentation (renal biopsy and nephrologic functional diagnosis). This case suggests that benign hypertension does not cause renovascular damage and renal failure. Plasma renin activity was found to be basically elevated and, furthermore, stimulated by e.g., dialysis. However, this single case does not permit any conclusions about a pathogenetic role of renin in creating hypertension by e.g., renal vasoconstriction or despite hypertension - collapse of the capillary network.
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PMID:[Renal thrombotic microangiopathy with benign hypertension and uremia secondary to oral contraceptives (author's transl)]. 97 70

The renal histopathology of essential malignant phase hypertension in two groups of black South Africans was studied. The first, an autopsy series, consisted of material obtained in 1956-1961, a period when adequate antihypertensive therapy had not yet become generally available. The second group, a renal biopsy series, was from an era when effective antihypertensive therapy was available (1979-1989). The study showed that the clinical and histopathological changes of malignant hypertension were similar in both the pre-treatment and treatment eras. Fibrinoid necrosis was found in 92% of the autopsy sections and 44% of the biopsies. While mucinous, onion-skin and fibrotic changes of the blood vessels were commonly found, they were not invariably present and could not be considered the histopathological hallmark of malignant nephrosclerosis. It was often impossible on histological examination to distinguish malignant nephrosclerosis arising de novo from that superimposed on long-standing previous benign hypertension. Replication of internal elastic lamina, which has been considered a marker of long-standing previous benign hypertension, was a nonspecific finding and was frequently observed in young hypertensive subjects with a short clinical history. When fibrinoid necrosis is present, diagnosis of malignant nephrosclerosis can be made with confidence in black South Africans.
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PMID:The renal histopathology of essential malignant hypertension in black South Africans. 187 49

To assess the hemodynamic characteristics in malignant hypertension, echocardiography was performed in 18 patients with malignant essential hypertension (MH-I, n = 9) and secondary hypertension (MH-II, n = 9). Patients with benign hypertension with or without left ventricular hypertrophy (n = 8 and 7, respectively), patients with hypertensive heart failure (n = 7) and normotensive volunteers (n = 10) were subjected to controls. Plasma noradrenaline (NA) and renin activity (PRA) were also measured prior to the antihypertensive therapy. There were no significant differences in the durations of hypertension before the malignant phase, and the mean arterial pressure between MH-I and MH-II. Although posterior wall thickness (PWTd) in MH-II was similar to that in MH-I, interventricular septal thickness (IVSTd) was less marked in MH-II. The plasma NA and PRA were markedly increased in both MH-I and MH-II. End-diastolic dimension (Dd) of the left ventricle was within normal range, but end-systolic dimension (Ds) was significantly increased in MH-I, MH-II and hypertensive heart failure. The moderate decreases in ejection fraction (EF) and mean velocity of circumferential fiber shortening (mVcf) were observed in both MH-I and MH-II. Marked decreases in EF and mVcf were also observed in patients with hypertensive heart failure. The relationship between systolic blood pressure and Dd/PWTd was shifted toward the right and upper portion of the normal relation in MH-I and MH-II. The present study demonstrated that the hemodynamic characteristics in malignant hypertension are an inappropriate left ventricular hypertrophy due to a marked increase in systolic stress; dilatation of the left ventricle in systole; and a moderate decrease in ventricular systolic function. It is suggested that a decrease in left ventricular systolic function in malignant hypertension might be due in part to a marked increase in the influence of neurohumoral factors on hemodynamics.
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PMID:[Echocardiographic features of left ventricular hypertrophy and contractility in malignant hypertension]. 253 Mar 33

Electrophoretic profiles of the molecular weight distributions of fibrinogen derivatives in blood provide a tool for combined assessment of coagulation and fibrinolysis in the course of vascular disease. Profiles obtained in studies on an experimental model of hypertension and in humans with occlusive vascular disease are discussed. In the experimental studies elevations in the level of cross-linked dimers provided a more reliable means for predicting development of malignant hypertension than did many other criteria, especially near the outset when blood pressure changed to similar degrees in rats with malignant and benign hypertension. Similarly, we find that levels of dimeric and occasionally trimeric forms of fibrinogen are more prominently elevated than degraded forms of fibrinogen in patients with occlusive vascular disease.
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PMID:Malignant hypertension, fibrinoid deposition, and fibrinogen electrophoresis. 266 31

Malignant hypertension is an important cause of morbidity and mortality among urban black South Africans. Hypertension accounts for 15.9% of all patients and for 34.6% of blacks receiving treatment for end-stage renal failure. Malignant hypertension is more commonly diagnosed than benign hypertension and two-thirds of patients present in the age group 30 - 49 years. Together they are the most common preventable cause of end-stage renal failure in this country. Acute partially reversible renal failure occurs in 20% of patients with malignant hypertension who require dialysis. This is an important subgroup, who may be recognised by their younger age, female preponderance and fulminant presentation. Short-term peritoneal dialysis and effective control of blood pressure will result in satisfactory return of renal function. However, only adequate country-wide control of hypertension will prevent these costly renal complications.
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PMID:Malignant hypertension and its renal complications in black South Africans. 266 74

To clarify predisposing factors for malignant hypertension, we retrospectively investigated the histories of 39 patients with malignant hypertension and 39 patients with benign hypertension. Between the malignant and benign groups, there was a statistically significant difference in blood pressure but not in age when hypertension was first noticed. The number of patients who had discontinued drug treatment was significantly greater in the malignant group (19; 49%) than in the benign group (11; 28%). Insufficient sleep, overwork, and/or mental burden of long duration were factors noticed within one year before the occurrence of the malignant phase in 11 (37%) of the 30 patients in that group in whom this information was available. Patients in the malignant group tended to belong to a lower social class. These results suggest that severe hypertension from an early phase, interruption of drug treatment, and physical and/or mental burden may predispose to the development of malignant hypertension, and that these predisposing factors are likely to be associated with social class.
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PMID:Predisposing factors for the development of malignant essential hypertension. 366 3

The role of circulating humoral agents in the pathogenesis of abnormal vascular wall cation composition in benign and malignant renal hypertension was investigated. Male F344 rats with chronic benign (n = 38) and malignant (n = 44) one-kidney, one clip (1K1C) hypertension and normotensive control rats (n = 63) were studied. Malignant hypertension developed spontaneously and was characterized by failure to thrive, weight loss, oedema, renal insufficiency, anaemia or haemoconcentration and hyperkalaemia. For bio-assay, monolayers of quiescent vascular smooth muscle cells from F344 rats were incubated in plasma or plasma extracts of normotensive and hypertensive rats for measurement of labelled rubidium (86Rb) uptake in the presence and absence of 2 mmol/l ouabain and/or 1 mmol/l furosemide. Compared with controls, ouabain-sensitive Rb uptake of cells was reduced in plasma extracts but not in whole plasma of rats with benign hypertension. Ouabain-sensitive Rb uptake was unchanged and ouabain-insensitive Rb uptake was reduced in both plasma and plasma extracts of rats with malignant hypertension. The latter was due to a reduction in furosemide-sensitive Rb uptake. In malignant hypertension, the increased sodium (Na) content of the aorta which characterizes benign hypertension was reversed and bladder wall Na content was reduced. The findings suggest that in malignant hypertension a circulating, furosemide-like inhibitor of ouabain-insensitive cation transport is the cause of vascular wall Na depletion and of diuresis and natriuresis that trigger the syndrome.
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PMID:Different cation transport inhibitor in benign and malignant experimental renal hypertension. 379 32

A diagnosis of malignant hypertension was recorded for 165 patients in the national morbidity study between 1970 and 1973. Three patients with benign hypertension were selected as age- and sex-matched controls for each case. The general practitioners in the study were asked to complete a further questionnaire about the patients and 66% of the practices agreed to take part. Information about the retinal findings for the patients was requested and less than half of those in the national morbidity study proved to have a strict diagnosis of accelerated or malignant hypertension although they were originally recorded as patients with malignant hypertension. Of those patients originally classified as having benign hypertension 5% had the retinal appearance of accelerated or malignant hypertension.Patients had been diagnosed as having hypertension for a mean of more than five years prior to entry into the national morbidity study and the survival of patients with both benign and accelerated or malignant hypertension was good. Thirtyfour per cent of those with confirmed benign hypertension and 62% of those with definite accelerated or malignant hypertension died in the follow-up period which was on average 10 years from entry into the national morbidity study.The survival of patients registered with doctors who did not collaborate and of patients whose clinical details were missing was similar to the survival of patients for whom full details were provided.Blood pressure control was only fair with a mean of 172/101 mmHg for the group with benign hypertension and 177/107 mmHg for the group with accelerated or malignant hypertension. Blood pressure control was the poorest for those who died from a stroke. A high proportion (78%) of deaths in association with accelerated or malignant hypertension were from cardiovascular or renal causes.
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PMID:Malignant hypertension in general practice. 407 97


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