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

1. Restriction of dietary salt intake does not affect the development or maintenance of hypertension in rats with unilateral renal ischaemia whether the contralateral kidney is present (Goldblatt 2 model) or not (Goldblatt 1 model). 2. Acute dietary salt depletion induces a similar loss of sodium and fall in body weight with little change in blood pressure in both normal and hypertensive rats. 3. Excision of the ischaemic kidney in rats with short-term (less than 50 days) Goldblatt 2 hypertension restores the mean blood pressure to normal, whereas Goldblatt 1 hypertensive rats show only a partial response. Previous salt depletion of this model enhances the blood pressure response to nephrectomy. 4. Sodium retention plays no part in the development or maintenance of Goldblatt 2 kidney hypertension. However, although sodium retention is normally involved in the Goldblatt 1 model, hypertension can develop in the absence of dietary sodium.
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PMID:Influence of sodium restriction upon two models of renal hypertension. 96 57

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

Several methods were used in an attempt to produce preeclampsia in the pregnant rat. Desoxycorticosterone acetate plus increased NaCl intake produced hypertension, proteinuria, rapid weight gain, convulsions, decreased litter size, decreased offspring weight, increased fetal and maternal mortality, and renal lesions similar to those seen in human preeclampsia. Injection of placenta in Freund's adjuvant produced mild blood pressure elevation and proteinuria in the pregnant rat. Rabbit antirat placenta serum produced hypertension in the pregnant rat but not in the nonpregnant rat. Liver congestion and renal glomerular congestion were observed in both pregnant and non-pregnant rats. Pregnancy in the rat reduced hypertension produced by applying a Goldblatt clamp prior to breeding. Uterine ischemia produced by wrapping the uterus in cellophane produced mild blood pressure elevation and proteinuria. A vitamin-E-deficient diet that contained substantial amounts of partially perioxidized, polyunsaturated fatty acids produced morphological lesions in the pregnant rat similar to those seen in human preeclampsia, but hypertension, edema, and proteinuria were absent. None of the maneuvers was effective in producing a complete model of human preeclampsia, but they do provide material for study that could answer somebasic questions about preeclampsia.
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PMID:The rat as a model for preeclampsia. 100 52

The realtionship between in vitro prostaglandin production by renal medullary tissue and hypertension was investigated in three models of hypertensive rat, i.e., DOCA, Goldblatt and SHR. Medullary minces were incubated for 30 minutes. Following incubation tissue PGE2 concentration was quantified using mass fragmentography. Media PGE2 concentrations were quantified using radioimmunoassay. Concentrations of PGE2 in tissue from Goldblatts and SHRs were significantly less than normotensive controls. The concentration of PGE2 in media after incubating SHR tissue was significantly less than normotensives. The data suggest that alterations in PGE2 metabolism are similar in Goldblatt and SHR hypertension.
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PMID:Prostaglandin E2 production by renomedullary tissue of DOCA, Goldblatt and spontaneously hypertensive rats. 100 18

Involvement of the area postrema in experimental hypertension has been investigated. Ablation of the rear apex of the fourth brain ventricle (=the region of the area postrema) elevated blood pressure, heart rate and plasma angiotensin II level. The same characteristic changes were seen in the two kidney Goldblatt rat model of hypertension. A possible involvement of the area postrema in this model of hypertension is discussed. Intraventricular perfusion of angiotensin II elevated blood pressure without a significant change in heart rates. This pressor response appeared to be dependent on release of antidiuretic hormone. The results are discussed in relation to the intrinsic brain angiotensinogenase system.
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PMID:Central pressor actions of angiotensin II. 103 May 65

1. Infusion of angiotensin II antagonist failed to restore the blood pressure of short-term Goldblatt 2-kidney hypertensive rats to normal levels before and after sodium restriction. 2. The blood pressure of both normal and sodium-restricted Goldblatt 2 hypertensive rats remained elevated 6 h after bilateral nephrectomy. 3. The residual hypertension found during antagonist infusion and after bilateral nephrectomy is not maintained by the renin-angiotensin system or sodium retention.
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PMID:The role of sodium retention in Goldblatt 2-kidney hypertension in the rat. 107 86

1. In forty-one patients who underwent renal homotransplantation the following measurements were made: (a) blood flow and its distribution in the transplanted kidney as measured by the 85-Kr washout method; (b) renin release in the renal vein of the transplant; (c) arteriovenous difference in plasma renin activity (PRA) of the recipient's remaining left kidney. 2. Eleven transplanted patients were normotensive. Renal haemodynamic data were comparable with those obtained in potential kidney donors. 3. Three hypertensive patients had chronic rejection. The mean renal blood flow and the percentage flow in the first component of the washout curve were reduced. Renin release from the transplant, however, was normal. 4. Ten hypertensive patients had transplant artery stenosis. In eight of them renin release from the grafts as well as peripheral PRA were within normal range. This result is similar to experimental data obtained in Goldblatt renovascular hypertension. The two patients with the tightest artery stenosis had an elevated renin release from the transplant. 5. Thirteen hypertensive patients had elevated arteriovenous difference in PRA of the recipient's own left kidney. Peripheral PRA was significantly higher than in normotensive patients. Left nephrectomy relieved hypertension in ten of them; three have not so far undergone nephrectomy. 6. In four other cases hypertension was also relieved by removal of the patient's own kidney; however, the arteriovenous difference in PRA of that kidney fell within normal range.
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PMID:Permanent hypertension after renal homotransplantation in man. 109 19

A fifty-seven-year-old patient with a five to one elevation of right renal vein plasma renin activity associated with a large, simple cortical cyst of the right lower pole is presented. Marsupialization of the cyst was associated with improvement in the patient's hypertension and the finding of bilaterally equal renal vein renin activity three months postoperatively. Possible mechanisms for hypertension are discussed in context of the experimental models of Goldblatt and Page in such lesions as cortical cysts of large size causing hydronephrosis, vascular stretching, or renal parenchymal compression.
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PMID:High renin hypertension associated with renal cortical cyst. 127 11

Altered erythrocyte Na+ transport has been observed in relation to the pathogenesis of essential hypertension. In the present study, intracellular Na+ and K+ levels, Na(+)-K+ pump activity, Na(+)-K+ cotransport, and Na+ passive permeability were measured in erythrocytes of DOC-salt hypertensive (DSH) rats, two-kidney, one clip Goldblatt hypertensive (2KH) rats, and spontaneously hypertensive rats (SHR). The results were as follows: 1. In comparison with the control groups, no change in the erythrocyte Na+ level was noted in the DSH and 2KH groups, whereas a significant increase was seen in the SHR group. 2. Although no change was noted in the erythrocyte K+ level in the 2KH and SHR groups when compared with the control groups, a significant decrease was seen in the DSH group. 3. Na(+)-K+ pump activity of erythrocytes was not changed in the DSH and 2KH groups when compared with the control group, but a significant increase was noted in the SHR group. 4. Na(+)-K+ cotransport of erythrocytes was not changed in any hypertensive rats when compared with the controls. 5. Na+ passive permeability in the erythrocyte membrane was not changed in the DSH and 2KH groups when compared with the control groups, but a significant increase was noted in the SHR group. These findings suggest that increased erythrocyte Na+ levels in SHR are due to increased Na+ passive permeability of the erythrocyte membrane, and increased Na(+)-K+ pump activity may be compensating for the increased intracellular Na+ concentration in erythrocytes. Furthermore, the increase in Na+ passive permeability observed in SHR might not result from hypertension itself but from abnormalities in the erythrocyte cell membrane, because no increase in Na+ passive permeability was noted in either DSH or 2KH rats.
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PMID:Erythrocyte sodium ion transport system in DOC-salt, Goldblatt, and spontaneously hypertensive rats. 132 86

In the present study, arteriosclerotic change of the aorta was induced in rats. The effects of manidipine hydrochloride on the resulting hypertension and arteriosclerotic change were studied. In endothelium-injured cholesterol-fed Goldblatt 2K1C rats, moderate elevation of blood pressure was noted at 3, 4, and 5 weeks. Laboratory studies performed at the end of 6 weeks also showed hypercholesterolemia, accompanied by a reduction of triglycerides and HDL cholesterol. Regular doses of manidipine (200 or 500 mg/kg) resulted in a dose dependent inhibition of the blood pressure elevation and a reduction of HDL cholesterol, but had no effect on cholesterol or triglyceride levels. Morphological studies in endothelium-injured rats afflicted with hypercholesterolemia and hypertension, showed medial thickening and intimal hyperplasia. Hyperplasia of the intima was a result of excessive proliferation of the smooth muscle cells. These cells showed an unusually large number of fat droplets and were considered indicative of atheromatous plaque formation. In rats treated with manidipine, hyperplasia of the media was completely suppressed while hyperplasia of the intima was reduced by a minimum of 50%. This study demonstrated that hypercholesterolemia and hypertension produced arteriosclerotic change in endothelium-injured rats, which was inhibited by manidipine. It is not known whether antiarteriosclerotic action was involved in the antihypertensive effect of manidipine.
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PMID:Manidipine inhibits the progression of hypertension and atherosclerosis in endothelium-injured and cholesterol-fed Goldblatt 2K1C rats. 134 87


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