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

1. Propranolol was administered to groups of mature rats before and during the development of renal hypertension induced by ligation of the aorta between the renal arteries. 2. At a dose 10 mumol (3 mg) of propranolol/kg, administered by intraperitoneal injection, the onset and severity of hypertension were not affected, although plasma renin concentration was significantly lower than in the untreated hypertensive rats in the first 5 days after the operation. 3. With 200 mumol (60 mg) of propranolol/kg, administered in the drinking water, peak blood pressure 5 days after aortic ligation was lower than in the untreated control rats, but plasma renin concentration was no lower than with the smaller dose. 4. The development of severe hypertension despite reduction in plasma renin concentration on the low dose of propranolol suggests the participation of renal vasopressor factors other than renin in this model. 5. A higher dose of propranolol reduced the rise in plasma concentration to an equal extent but the rise of blood pressure at 5 days was also reduced, which supports this concept.
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PMID:Effect of propranolol on blood pressure and renin in renal hypertension in the rat. 60 59

Arterial hypertension was induced in experiments on rats by chronic injection of indometacin, an inhibitor of prostaglandin synthesis, combined with a salt load or unilateral nephrectomy. A twofold rise in arterial pressure, on average, was noted at the end of the 6th week of the inhibitor injection. The development of arterial hypertension following indometacin injection and a salt load led to reduced excretion of sodium and water, increased intravascular volume, and increased sodium content in the aortic wall. In the group of nephrectomized and indometacin treated animals, on the contrary, sodium and water excretion increased, intravascular volume diminished, and the content of sodium in the aortic wall decreased. Chronic injection of indometacin alone into intact animals did not lead to a rise of arterial pressure within the same periods of time and did not induce changes in the renal excretory function. It is presumed that disorder of water-salt homeostasis is one of the mechanisms of the increase in arterial pressure.
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PMID:[Role of prostagladin synthesis inhibitors in the development of arterial hypertension. II]. 63 11

Virgin and breeder, male and female, Sprague-Dawley rats were unilaterally nephrectomized and given 1% saline drinking water. Animals were injected i.p., twice daily, with a 10 mg/100 g body wt dose of the 11-beta hydroxylation inhibitor, Metyrapone. After 7 weeks of treatment, both the previously nonarteriosclerotic virgin rats and the breeder rats with pre-existing arteriosclerosis developed de nove, widely distributed, intimal hyalinization of their peripheral arteries along with myocardial fibrosis and hyalinization of their intramyocardial coronary arteries. The Metyrapone-treated animals developed severe hypertension with greatly elevated serum creatin phosphokinase, glucose, BUN and cholesterol levels. The adrenal glands, hearts, and kidneys were greatly hypertrophied, in keeping with Metyrapone-induced extra ACTH release and the hypertension-induced myocardial and renal histopathology. Uniparous, Metyrapone-treated, female rats manifested an unusually high incidence of saccular aneurysms of the aorta. It is suggested that the hypertension and the intimal hyalinization and other specific morphologic characteristics of the cardiovascular degenerative changes observed were directly related to excess production of mineralocorticoids, e.g., deoxycorticosterone.
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PMID:Metyrapone-induced cardiovascular degenerative changes in non-arteriosclerotic and arteriosclerotic rats. 63 31

Renal clearance studies were performed in conscious 13-week-old spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY) before and during volume expansion by intravenous infusion of isotonic saline. Mean arterial pressure and filtration fraction were greater in SHR, whereas fractional and absolute excretion of sodium and water, glomerular filtration rate, and renal plasma flow in SHR and WKY were not statistically different. This was the case during hydropenia and volume expansion. We did not observe as exaggerated natriuresis after intravenous loading when unanesthetized SHR were compared with the response of WKY. These observations suggest that the kidneys of genetically hypertensive rats of the Okamoto-Aoki strain have adapted to an elevated renal perfusion pressure or that hypertension is required to normalize renal function so that excretion is appropriately matched with intake.
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PMID:Renal function of conscious spontaneously hypertensive rats. 63 95

Urinary kallikrein was measured in rats bred to be susceptible (S) or resistant (R) to the hypertensive effect of salt. To determine kallikrein, three different methods were used: (1) a new direct radioimmunoassay (RIA) for the enzymic protein: (2) a method based on the capability of kallikrein, when incubated with kininogen, to generate kinins which were then measured by RIA (kininogenase activity); and (3) a method based on the capability of kallikrein to break the ester bond of p-tosyl-L-arginine methyl ester (HCl (TAMe). A significant correlation ( r = 0.90) was found between the direct RIA and the kininogenase method. It was found that urinary kallikrein was significantly decreased in the S as compared to the R rats by the use of these three methods. Urinary kallikrein in the S rats was much lower when measured by the kininogenase method than by direct RIA or esterolytic assay. This difference could be due to excretion of pre-kallikrein and/or kallikrein bound to an inhibitor (inactive kallikrein). It is suggested that the decrease of urinary kallikrein excretion (active and inactive) in the S rats could be a consequence of a genetic defect that may affect the development of hypertension perhaps through the alteration of sodium and water excretion by the kidney.
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PMID:Urinary kallikrein in rats bred for their susceptibility and resistance to the hypertensive effect of salt. A new radioimmunoassay for its direct determination. 63 96

A laboratory model was developed in the dog to quantitate the effects of cerebral venous hypertension on inappropriate antidiuretic hormone (ADH) secretion. When cerebral venous pressure was abruptly increased during continuous water loading, there was a sharp rise in urine osmolality within 30 minutes. Urine osmolality continued to increase during, and ten minutes after, the period of hypertension. On lowering cerebral venous pressure, the osmolality returned to baseline within 60 minutes. The effects could be extended for at least three hours and presumably longer. A 50% response threshold for this ADH effect occurred at a cerebral venous pressure between 18 and 19 cm of water. The effect correlated with plasma ADH levels. The study paralled documented clinical observations. The results are discussed in light of the recognition and management of surgical states where increased cerebral venous pressure might produce a severe antidiuretic effect.
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PMID:Reduction of free water clearance with cephalic venous hypertension. 64 15

A case of meningococcal meningitis is described in which 10 days later there developed the histological lesions of acute exsudative proliferative glomerular nephritis without proteinuria, hematuria, hypertension or salt and water retention. The relationship between structural and functional changes in the kidney in glomerular nephritis is discussed in the light of these findings.
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PMID:Post meningococcal acute glomerular nephritis. 66 26

A 60-year-old woman who had been instructed to increase her water intake because of nephrolithiasis developed the syndrome of inappropriate secretion of antidiuretic hormone when treated with chlorthalidone for mild hypertension. Serum osmolality was 235 mOsm/kg with concomitant urine osmolality of 490 mOsm/kg. When serum sodium decreased to 110 mEq/liter, plasma antidiuretic hormone (ADH) was elevated at 30 pg/ml. The syndrome resolved when chlorthalidone was discontinued together with fluid intake restriction. Plasma ADH returned to normal (less than 0.5 pg/ml) after three days of treatment. The favorable outcome in this patient is attributed to early recognition of the syndrome, which might occur even with nonthiazide diuretics such as chlorthalidone.
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PMID:Chlorthalidone-induced syndrome of inappropriate secretion of antidiuretic hormone. 67 Apr 29

1. Male Wistar rats were housed individually in glass metabolic cages for 5 days during which time their food and water intakes reached plateau levels and they developed a significant systolic arterial hypertension. 2. After the initial 5-day period, systolic blood pressure and water and electrolyte balances were measured for 4 days before and 7 days after I.P. injection of 6-hydroxydopamine (100 mg/kg). In a separate experiment, plasma renin activity and glomerular filtration rate were measured 1 and 3 days after injection of 6-hydroxydopamine. Haematocrit, plasma volume, osmolality and plasma concentrations of glucose, sodium, potassium and protein were also measured at intervals after treatment. 3. Systolic blood pressure fell within 24 hr after treatment with 6-hydroxydopamine but was restored to pretreatment levels within 7 days. There was also a transient fall in glomerular filtration rate. 4. Plasma volume was significantly expanded on the first day after treatment and there was a fall in haemotocrit together with changes in plasma constituents indicative of a haemodilution, although plasma glucose levels were elevated. 5. There was a significant water retention on the third, fourth and fifth days after treatment but this was not accompanied by any measurable sodium retention and could not be attributed to renal compensation. Furthermore, plasma renin activity showed no significant change following 6-hydroxydopamine treatment. 6. It is suggested that the return of systolic blood pressure to pre-treatment levels was chiefly due to the return of vasoconstrictor function. The changes in plasma composition and volume were probably due to a fall in capillary hydrostatic pressure and an increase in the osmolality of extracellular fluid due to the elevated glucose levels.
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PMID:Reversal of 6-hydroxydopamine-induced hypotension in the rat without activation of the renin-angiotensin system. 67 44

Acute hypertension leads to alternating regions of dilation and vasoconstriction of surface cerebral vessels. It remains to be determined conclusively if either or both of those calibre changes are essential in the production of degenerative vascular changes of malignant hypertension. There is no evidence of ischemic or other morphologic change to components of the blood-brain barrier including the interendothelial tight junctions which remain intact. An early phase of evolving cerebral edema is swelling of astrocytic foot processes that occurs only in regions of abnormal protein permeability. The cortical location of these acute hypertensive lesions stands in contrast to the ganglionic location of the microaneurysms found as complication of chronic hypertension in man. The location of permeability changes to protein do not necessarily reflect changes in brain water permeability susceptible to sympathetic regulation.
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PMID:Hypertension and the blood-brain barrier. 67 98


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