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

1 The role of monoamine oxidase (MAO) in the maintenance of deoxycorticosterone-sodium chloride (DOCA-salt) hypertension was investigated by assaying the MAO activity both in central as well as peripheral blood vessels and in brain tissue. 2 The results suggest that the activity of MAO in the DOCA-salt hypertensive rat is similar to the activity present in the normotensive rat.
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PMID:Brain and vascular monoamine oxidase activity in the deoxycorticosterone-salt hypertensive rat. 84 81

The effect of hypertension, which is known to enhance atherosclerosis, on acid esterase activity of rat aortic wall was studied histochemically. The purpose was to test our notion that atherogenesis depends on the balance between supply of lipids to the arterial smooth muscle cells and the lysosomal esterase activities. Hypertension was produced in rats by unilateral nephrectomy and administration of desoxycorticosterone acetate and sodium chloride. The animals reacted with varying degrees of hypertension. In rats with hypertension of a sufficiently high degree and of long duration, inhibition of aortic acid esterase activities occurred. No inhibition of these enzymes occurred in the other organs examined.
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PMID:Experimentally produced hypertension and aortic acid esterase. 98 72

Unilaterally nephrectomized rats treated with deoxycorticosterone and 1% sodium chloride in their drinking water developed severe systemic hypertension with marked cardiac and renal lesions. No pathologic changes could be detected in the retinal vasculature by light microscopy, but electron microscopy revealed inconstant alterations in the pericytes of retinal capillaries: these cells showed hyaloplasmic edema, margination of chromatin, dilatation of rough endoplasmic reticulum, and swelling of mitochondria. Injection of lanthanum into control rats confirmed that this 40-A tracer cannot pass the interendothelial tight junctions. In hypertensive animals, however, it penetrated these junctions and could be visualized in capillary basement membranes and between cells of the retina. The results indicate that an increase in permeability is probably the first pathologic change to occur in the retinal capillaries of hypertensive rats.
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PMID:The retinal capillaries of the rat in deoxycorticosterone hypertension. An ultrastructural study with the diffusion tracer lanthanum. 99 22

1. The metabolic role of arterial angiotensin I-forming enzyme (i.e. renin activity) was studied in total homogenates and in subcellular fractions of the aorta of normotensive and hypertensive rats. 2. Angiotensin I-forming enzyme was measured in (a) uninephrectomized rats rendered hypertensive with D-aldosterone and sodium chloride (10 g/l drinking solution, (b) rats treated in the same manner but with the addition of spironolactone, and (c) control rats. 3. Hypertension developed in aldosterone-treated rats within 3-6 weeks and was associated with decreased plasma and renal renin values. Total aortic renin activity was up to sixfold higher in the hypertensive animals than in control animals and there was an increased ratio of supernatant to microsomal renin activity in the aorta. 4. In spironolactone-treated rats blood pressure and total aortic renin concentrations were comparable with those in the control rats. 5. The results support the hypothesis that renin generated at local vascular sites, which is independent of circulating renin levels, contributes to regulation of blood pressure.
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PMID:Effects of aldosterone and spironolactone on arterial renin in rats. 107 85

1. Bilateral compression of adrenal glands combined with unilateral nephrectomy and followed by imposition of a high sodium chloride intake caused severe hypertension in all rats, accompanied by enlargement of the heart, kidneys and adrenal glands, atrophy of the thymus and severe nephrosclerosis. 2. Digitoxin treatment delayed the onset, reduced the incidence and ameliorated the magnitude of the hypertensive response in such rats; it also reduced the degree of cardiac hypertrophy, the severity of nephrosclerosis and completely prevented enlargement of the adrenals and kidneys or atrophy of the thymus.
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PMID:Delayed onset and reduced severity of adrenal-compression hypertension in rats treated with digitoxin. 107 96

1. Oral administration of DL-alpha-tocopheryl nicotinate (EN) (0-04 or 0-2 mmol day-1 kg-1) or DL-alpha-tocopharyl acetate (EA) (0-2 mmol day-1 kh-1) delayed the progress of hypertension in unilaterally nephrectomized rats, which were treated with deoxycorticosterone and salt, and in genetically hypertensive rats (SHR) which were given sodium chloride solution. Suppression of body weight gain, incidence of pneumonia and mortality were reduced by treatment with EN or EA. 2. Severe hypertension in old SHR (9 months) further progressed, when drinking water was replaced by sodium chloride solution, and four out of ten of these animals died of cerebral haemorrhage during 4 weeks. The administration of EN or EA prevented the increase in blood pressure and incidence of stroke.
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PMID:Anti-hypertensive action of DL-alpha-tocopharyl esters in rats. 107 97

1. The role of renal medullary prostaglandin E has been examined in rats with hypertension induced by sodium chloride and deoxycorticosterone (salt-DOC). 2. Synthesis of prostaglandin E was normal in early salt-DOC hypertension. Indomethacin exacerbated the hypertension, and depressed synthesis of prostaglandin E equally in hypertensive and control rats. 3. Synthesis of prostaglandin E was depressed in rats with late salt-DOC hypertension. 4. The results lend support to the concept that prostaglandin E is involved in the regulation of arterial pressure.
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PMID:Renal prostaglandin synthesis in hypertension induced by deoxycorticosterone and sodium chloride in the rat. 107 21

1. Complete ligation of the aorta between the origins of the two renal arteries in the rat produces a predictable form of accelerated hypertension. Changes in the blood pressure, plasma renin activity and renal histological lesions have been studied. 2. Group 1 rats and their control group (group 2) received tap water, and group 3 and its control group (group 4) received sodium chloride solution (0-154 mol/l) in place of tap water, for 4 weeks before aortic ligation. In the experimental groups 1 and 3, complete ligation was carried out. In groups 2 and 4 the aorta and renal arteries were exposed, but not ligated. Interlobular artery lesions were studied on a blind basis and graded 0-4 according to severity. 3. Groups 1 and 3 developed severe hypertension. In group 1 the raised mean arterial pressure showed a significant correlation with increased plasma renin activity. Both mean arterial pressure and plasma renin activity also showed a significant correlation with changes in interlobular arteries. In group 3 the raised mean arterial blood pressure did not show a significant correlation with the depressed plasma renin activity, or with changes in interlobular arteries. A significant correlation was, however, found between plasma renin activity and interlobular artery lesions in group 3. 4. These results suggest that the renin-angiotensin system may influence renal vascular lesions through some mechanism independent of the blood pressure.
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PMID:Accelerated hypertension in the rat: relation between renin, renal vascular lesions, salt intake and blood pressure. 107 10

1. The mechanism by which pretreatment of rats with intracisternal 6-hydroxydopamine prevents the onset of deoxycorticosterone hypertension has been studied. 2. Rats pretreated with central 6-hydroxydopamine increase their consumption of 0-17 mol/l sodium chloride--0-03 mol/l potassium chloride ('saline') less than normal rats when implanted with deoxycorticosterone. 3. Intact rats restricted to the equivalent consumption of saline of rats pretreated with 6-hydroxydopamine develop hypertension despite this restriction. 4. It is suggested that the prevention of deoxycorticosterone hypertension by central 6-hydroxydopamine does not depend on reduced saline consumption.
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PMID:Role of saline consumption in the prevention of deoxycorticosterone hypertension in rats by central 6-hydroxydopamine. 112 24

Further studies are reported on the existence of a sensitizing factor in plasma of hypertensive subjects, which increases the vascular sensitivity to pressor agents when injected iv into nephrectomized rats. Plasma samples from normotensive subjects, patients with malignant hypertension, normotensive dogs, and dogs with experimental renovascular hypertension were fractionated on Bio-Gel P-10 columns after cold acetone precipitation, and on DEAE-cellulose columns eluted with sodium chloride and pH gradients. The effect of the various fractions on the vascular sensitivity to angiotensin was tested utilizing nephrectomized rats. The sensitizing activity was found only in fractions obtained from plasma of hypertensive patients and dogs and it was concentrated primarily in three fractions. Th results suggest that the sensitizing factor is negatively charged at neutral pH and it could be a polypeptide or a small protein.
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PMID:Further studies on the existence of a sensitizing factor to pressor agents in hypertension. 115 Aug 66


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