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

The theory of whole body autoregulation to explain the pathogenesis of experimental renal hypertension states that hypertension is initiated in response to an early increase in salt and water retention and a subsequent elevation of the cardiac output. This hypothesis was evaluated in the present study. Dogs (n,5) were made hypertensive by wrapping the left kidney in cellophane and removing the contralateral kidney 3 wk later. One week prior to right nephrectomy, the dogs were volume depleted by placing them on a low sodium intake (less than 3 meq of sodium/day) and giving them a mercurial diuretic for the first 3 days of the diet. This superimposed sodium depletion (negative sodium balance of 137 +/- 17 meq) increased plasma renin activity 3-5 times but did not change arterial pressure or heart rate. Within 2 days after nephrectomy, the mean arterial pressure increased from the control level of 105 +/- 1 to 135 +/- 6 mmHg (P less than 0.005) and pressure remained elevated throughout an additional 4-wk period in which volume depletion was enforced. The present study suggests, therefore, that initial blood volume expansion with such possible consequences as elevated cardiac output are not essential to the pathogenesis of experimental renal hypertension.
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PMID:Development of chronic perinephritic hypertension in dogs without volume expansion. 91 Sep 53

Inverse interrelations between plasma renin activity and exchangeable sodium or blood volume were found in both normotensive (N = 23) and hypertensive (N =29) hemodialysis patients (r= 0.47; P less than 0.005); however, mean plasma renin for any given sodium/volume state was at least two-fold higher in hypertensive than in normotensive hemodialysis patients or normal subjects (N =31). In the hemodialysis patients, blood pressure correlated weakly but significantly with the products of circulating renin and exchangeable sodium (r=0.37; P less than 0.005) or blood volume (r = 0.29; P less than 0.05). Multiple regression analysis including duration of previous hypertension as the second independent variable increased these correlation coefficients to 0.44 and 0.42, respectively. This suggests that hypertension in endstage kidney disease is often associated with resetting of the body sodium/fluid=renin feedback mechanism. Inappropriately increased plasma renine activity relative to the body sodium/volume state as well as high blood pressure-induced vascular changes may play important complementary roles, but it appears evident that additional mechanisms are also operative in maintaining end-stage renal hypertension.
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PMID:Hypertension in terminal renal failure. 94 Feb 71

Patients with chronic glomerulonephritis and mild hypertension show a consistent behaviour in their renin-aldosterone-system. There is a close correlation between the elevation of mean blood pressure and destruction of glomeruli. No correlation has been found between renin values and the degree of hypertension. Thus the cuase of mild hypertension occurring in the early stages of chronic GN remains to be elucidated. Normal PRA values in spite of hypertension and expansion of ECFV accompaning progression of chronic glomerulonephritis could be a sign of "relative hyperreninemia". Apparently various mechanisms are involved in the pathogenesis of renal hypertension. These include sodium retention, increased cardiac output. anemia, renin, aldosterone, prostaglandins, expanded plasma volume and peripheral vasoconstriction. These factors are more or less active in the different stages of hypertension and renal failure.
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PMID:Plasma renin activity (PRA) and aldosterone (PA) in patients with chronic glomerulonephritis (GN) and hypertension. 94 54

The effect of chronic renovascular hypertension on the autoregulation of cerebral blood flow was studied in anesthetized baboons. Cerebral blood flow was measured by the intracarotid 133Xe clearance method. Six baboons with renal hypertension of 8-12 weeks' duration were compared with six normotensive controls. The lower limit of autoregulation was determined following controlled hemorrhage. In the initially normotensive baboons, cerebral blood flow remained constant until mean arterial pressure had decreased to the range of 45-59 mm Hg. Thereafter, cerebral blood flow decreased with each further decrease in mean arterial pressure. In the chronically hypertensive baboons cerebral blood flow autoregulated until the mean arterial pressure had decreased to the range of 75-89 mm Hg. Therefore, the lower limit of autoregulation of cerebral blood flow was shifted to higher absolute levels of mean arterial pressure in baboons with chronic renovascular hypertension presumably due to adaptive changes in the cerebral circulation.
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PMID:Lower limit of cerebral blood flow autoregulation in experimental renovascular hypertension in the baboon. 96 39

The content of total metabolizing sodium was studied in 74 patients with hypertension of different genesis, using the Na24-isotope dilution technique. Among these patients 31 had essential hypertension, 43--symptomatic hypertension (40--renal, and 3--adrenal). In Stage IB and IIA hypertension, a reduction of the level of total metabolizing sodium and its increased urine excretion were found. At late stages of essential hypertension, like in symptomatic renal hypertension, normal levels of total metabolizing sodium were found, or a slight tendency towards its elevation. In cases of adrenal hypertension (Conn's syndrome, pheochromocytoma) the level of total metabolizing sodium is significantly elevated. No correlation was seen between the levels of total metabolizing sodium, and plasma and erythrocytes sodium. The decrease of total metabolizing sodium at early stages of essential hypertension must be an adaptative reaction of the body, which is proved by the increased urine excretion of sodium.
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PMID:[Content of total metabolic sodium in arterial hypertension of varying origin]. 97 79

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

1. The hypothesis that suppression of prostaglandin E (PGE) synthesis by indomethacin exacerbates renal clip hypertension in the rat was investigated. 2. Indomethacin exacerbated hypertension in renal clip rats. 3. In vitro PGE synthesis determined by gas liquid chromatography (GLC) was suppressed in medullary tissue from the hypertensive animals irrespective of indomethacin treatment. 4. The findings support the concept that PGs participate in blood pressure regulation in experimental renal hypertension.
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PMID:Renal prostaglandin synthesis in experimental renal clip hypertension in the rat. 98 62

Selective renin sampling from renal vein tributaries identified a high-renin source in the lower pole of the left kidney in a 16-year-old boy who had gradually developed hypertension after blunt left renal trauma. Localized renin secretion from the ischemic pole was associated with suppression of renin secretion from both the contralateral kidney and the normal part of the affected kidney. Removal of ischemic tissue by partial nephrectomy produced sustained correction of hypertension. The findings indicate that segmental renin sampling can define indications for partial nephrectomy in renal hypertension.
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PMID:Segmental renin sampling and partial nephrectomy in renal hypertension. 98 90

Preliminary results of this retrospective-prospective analysis of renal hypertension in 110 children indicate that hypertension may be secondary to a wide variety of acute progresive, and chronic renal diseases which may be either congenital or acquired. Affected children may be detected at any time from infancy through adolescence. Symptoms usually associated with acute glomerulonephritis (i.e., headache, swelling, nausea, vomiting, anorexia, fatigue, dizziness, and fever) occur in both acute and chronic renal diseases associated with hypertension. Headache and swelling are the most common symptoms in this series. Peripheral edema, rales, and increased heart size were found in between 10 and 25% of these children. Differential diagnosis may be approached by a consideration of causes of acute and chronic hypertension. The child with chronic renal disease usually presents with a long history of fatigability, poor growth, and pallor, and laboratory tests reveal elevation of the creatinine and BUN along with anemia, hypocalcemia, and hyperphosphatemia. In contrast, the child with acute renal disease and hypertension presents with a history of prior good health followed by the abrupt onset of signs and symptoms of renal disease; laboratory tests usually reveal modest elevations of creatinine and BUN, anemia is unusual, an abnormal urinalysis is common, and serum calcium and phosphorous levels are usually normal. Renovascular and asymmetric renal parenchymal disease represent uncommon but important conditions because surgery may be curative. Treatment may be surgical, medical, or combined. Surgical conditions include renal trauma, hydronephrosis, asymmetric renal disease, and renal arterial disease. Adequate blood pressure control without medication can be expected following surgery in instances of unilateral involvement with a normal contralateral kidney. Meticulous assessment of the contralateral kidney is needed to determine that it is normal. If surgery is unsuccessful or is not indicated, pharmacologic therapy is initiated with a stepwise regimen starting with the mildest agent (e.g., thiazides) and then adding additional antihypertensive drugs when adequate blood pressure control has not yet been achieved. The goal of therapy is the lowest, safest, tolerated blood pressure levels. Long-term, carefully designed studies of antihypertensive agents for children with renal hypertension are not available. The need for collection and critical analysis of data concerning the clinical course of children with renal hypertension is evident from a review of the literature and from the preliminary data presented in this series. The presentation of such information and a critique of outcome variables will provide a basis for program planning for affected children and improvement in patient care where indicated.
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PMID:Renal hypertension in children. 99 44

The purpose of the investigation was to study the alterations in the lipid and lipoprotein content in the blood serum, the liver and the aortic wall of rats with experimentally induced salt, renal (Goldblatt) and adrenal-regeneration hypertension. The experiments were carried out on 59 Wistar rats (25 normotensive controls). It was established that both the serum and the liver lipid patterns vary in the three experimental models of hypertension. Thus, while in salt-induced hypertension no hyperlipidaemia and hyperlipoproteinaemia were established, in renal hypertension the serum lipid and lipoprotein levels were significantly increased in comparison to the controls. The cholesterol content in the liver was increased in all the three models of hypertension. The remaining lipid fractions were within normal ranges or a little decreased in salt-induced hypertension, while in renal and adrenal-regeneration hypertension their quantity was significantly increased. A two weeks' treatment with hypotensive prostaglandin E1 diminished the lipid and lipoprotein contents in the liver of rats with adrenal-regeneration hypertension, only cholesterol remaining unaltered. The blood serum level of free fatty acids increased in all the three models of experimental hypertension, as did the cholesterol and beta-lipoprotein level in the aortic wall. The alterations in lipid and lipoprotein metabolism established in this study are regarded as specific for the hypertensive process itself, since no histological alterations characteristic of atherosclerosis were observed.
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PMID:The action of arterial hypertension on lipid and lipoprotein metabolism. I. Salt, adrenal-regeneration and renal (Goldblatt) hypertension. 100 Sep 84


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