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

Fifty-five patients with mild to moderately severe essential hypertension were treated with guanabenz (2, 6-dichlorobenzylidene aminoguanidine acetate) in doses from 4 to 16 mg twice daily in a randomized, placebo-controlled study. The patients treated with placebo in the initial phase of the study were subsequently treated with guanabenz. The mean arterial pressure in the guanabenz group decreased from 130.6 to 107.6; that in the placebo group decreased from 129.6 to 126.6 standing and from 126.6 tp 109.9 and 128.8 to 120.5, respectively, supine. The principle adverse effects included sedation, dry mouth, weakness, and tiredness. Of the guanabenz-treated patients 84% had sustained decrease in supine diastolic blood pressure of 10 mm Hg or more, whereas in the placebo-treated patients only 32% had such a response. There was no significant orthostatic hypotension. Guanabenz thus appears to be an effective antihypertensive drug in patients with mild to moderately severe hypertension.
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PMID:Guanabenz in essential hypertension. 31 38

Changes in the fractional distribution of cardiac output (FF), organ blood flow, and regional vascular resistance were measured by the isotope dilution technique of Sapirstein using 86Rb as indicator in unanesthetized rats during acute arterial hypertension produced by bilateral lesions of the nucleus tractus solitarii (NTS). After NTS lesions, the FF was significantly reduced in skin, muscle, and colon, increased in ventricular myocardium, spleen, and adrenal glands, and was unchanged elsewhere. Because of a marked reduction in cardiac output (CO) during hypertension, the absolute organ blood flow (FF X CO) was reduced in lesioned rats to 30-40% of control in skin, muscle, and colon and between 60% and 75% of control in most of the remainder of the gastrointestinal tract and renal cortex; it was unchanged in myocardium and endocrine glands. Resistance was substantially increased (4- to 6-fold) in skin, muscle and colon but was only moderately increased (1.5- to 2.5-fold) in the remaining organs. The results indicate that, while NTS lesions will increase resistance in most vascular beds, the response is unequally distributed, influencing skin, muscle, and colon disproportionately to other tissues. Because of an interaction between a reduction in CO and little autoregulation, blood flow is reduced primarily in skin, muscle, and colon. The pattern of redistribution of CO was consistent with the interpretation that NTS hypertension results from interrupting baroreceptor reflexes centrally. The pattern of redistribution of blood flow in rats with NTS lesions differs from that produced by deoxycorticosterone acetate-salt and renal ischemia.
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PMID:Regional distribution of blood flow during arterial hypertension produced by lesions of the nucleus tractus solitarii in rats. 33 95

To define the role of the renin-angiotensin system in post-transplantation hypertension we studied 12 hypertensive recipients of renal transplants. The patients received saralasin acetate, an angiotensin II antagonist, while on a normal sodium diet and again after seven days of sodium restriction. In six patients with only one kidney, saralasin did not lower blood pressure on either diet; salt depletion did not lower systolic or diastolic blood pressures. In six patients with more than one kidney, salt depletion also did not lower blood pressure; however, salt depletion plus saralasin lowered their systolic pressures from a mean (+/- S.E.M.) of 146 +/- 9 to 128 +/- 8 mm Hg, and mean diastolic pressures fell from 103 +/- 5 to 89 +/- 5 (P less than 0.001). In four of five patients renal-vein renin activity was greater in one or more host kidneys than in the transplant kidney (or kidneys). Although pre-transplant blood pressure was the same in both groups, post-transplantation hypertension is more likely to be angiotensin II-dependent in patients with more than one kidney.
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PMID:Role of the renin-angiotensin system in post-transplantation hypertension in patients with multiple kidneys. 34 89

To characterize the renin-angiotensin system in the Aoki-Okamoto spontaneously hypertensive rat (SHR) more fully, serial measurements of plasma renin activity (PRA), plasma renin concentration (PRC), renin reactivity (as relative index of circulating modifiers of the renin reaction) and renin substrate concentration were made in 6- to 64-week-old SHR and in age-matched Wistar-Kyoto normotensive rats (WKY). In the evolving phase of SHR hypertension (6 and 13 weeks of age), PRA was comparable to WKY control values, whereas mature SHR with established hypertension developed, between 13 and 35 weeks of age, a high-PRA state persisting through 64 weeks of age. In 64-week-old SHR, increased plasma volume (3.54 +/- 0.91 in SHR vs. 3.18 +/- 0.90 ml/100 g body weight in WKY, p less than 0.025), together with increased PRA (24.9 +/- 3.8 in SHR vs. 13.1 2.2 ng AI/ml plasma/hr in WKY, p less than 0.025), suggest that volume decrease cannot explain increased PRA. In 42-week-old SHR, PRA was incompletely suppressed by deoxycorticosterone acetate plus 1% saline orally for 4 days: 4.9 +/- 1.2 in SHR vs. 0.6 +/- 0.8 ng angiotensin I/ml plasma/hr in WKY, p less than 0.001. Modestly increased renin reactivity of plasma was observed in SHR at all ages studied, supporting the ubiquity of increased circulating accelerators (or decreased inhibitors) of the renin reaction in hypertensive states. However, elevated renin reactivity did not account for the transition from normal to high PRA observed in mature SHR, nor did renin substrate concentration, which was consistently lower in SHR than in age-matched WKY. Temporal patterns of, and strain differences in PRA were closely paralleled by variations in PRC but not by other reaction components. Significant elevation of serum creatinine in old SHR support the presence of renal injury. We conclude that PRA and PRC are normal in evolving SHR hypertension and progress to abnormally elevated levels after hypertension is established. We postulate that "high-renin" hypertension may develop as a consequence of the hypertensive state per se, perhaps due to nephrosclerotic vascular disease.
Hypertension
PMID:Serial renin-angiotensin studies in spontaneously hypertensive and Wistar-Kyoto normotensive rats. Transition from normal- to high-renin status during the established phase of spontaneous hypertension. 39 38

Measurements of precapillary resistance (Ra), postcapillary resistance (Ra), postcapillary resistance (Rv), capillary filtration coefficient (Kf), and mean capillary hydrostatic pressure (Pci) were made during constant-flow perfusion of isolated hindlimbs from control and deoxycorticosterone acetate (DOCA)-NaCl-treated hypertensive dogs by the isogravimetric method. Both Ra and Rv were found to be significantly increased in the hypertensive group, even after maximal vasodilatation with papaverine. The net decreases in Ra and Rv following papaverine infusion were not significantly different between control and hypertensive animals. These results suggest that the observed increases in Ra and Rv were due to structural adaptation (increased wall-to-lumen ratio). Nonpapaverinized hindlimbs from hypertensive dogs exhibited a significant 40% reduction in Kf, suggesting that capillary surface area for fluid exchange was decreased. The compliance of the hindlimb vascular bed was found to be significantly decreased in the hypertensive group. Pci of both groups of hindlimbs were not different between groups and was not affected by papaverine. This result suggests that net capillary permeability to plasma proteins in this preparation was not changed by hypertension.
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PMID:Effect of DOCA-NaCl hypertension on pre- and postcapillary resistance in isolated hindlimbs of dogs. 43 24

Hypertension was induced in rats (Hebrew University strain) by three different procedures: (1) deoxycorticosterone acetate (DOCA)--salt treatment; (2) unilateral renal artery clip or (3) chronic salt-loading. Noradrenaline (NA) and dopamine (DA) distribution in different brain areas was assayed following induction of hypertension. NA content increased significantly in various areas: the increase of NA in the pons-medulla was common to all procedures inducing hypertension. NA content increased also in the mesencephalon, the hypothalamus and the rest of the forebrain (DOCA--salt hypertension), in the mesencephalon, the hypothalamus and the cortex (in renal clip hypertension). No significant changes in DA content were observed in any region of the brain following induction of hypertension by the three different methods. In two substrains, selected from the Hebrew University strain, for their respective sensitivity (H) or immunity (N) to hypertension induced by DOCA--salt treatment, there were no significant increases in NA or DA in any part of the brain following DOCA--salt treatment. Comparison of NA concentrations in these strains showed that NA was significantly higher in the pons-medulla of the untreated N strain rats than in the medulla of untreated H strain or in untreated rats of the original strain (Hebrew University). A model is presented suggesting that central NA-containing neurons plays a major role in controlling hypertension.
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PMID:Experimental hypertension and catecholamine distribution in the rat brain. 46 31

1. The Carworth Long-Evans rat has been reported to develop adrenal-regeneration hypertension but not deoxycorticosterone acetate (DOCA) hypertension. Deficiency of a hypothalamic receptor for deoxycorticosterone which mediates saline polydipsia has been postulated to underlie this resistance. Since a mineralocorticoid etiology for adrenal-regeneration hypertension has been postulated and all mineralocorticoids are thought to act on common receptors, these previous reports are difficult to reconcile. 2. To determine if an absolute or relative resistance to mineralocorticoids is present, Charles River Long-Evans and Sprague-Dawley rats were given 40 mg (107 micromol) of DOCA pellets/rat or 250 microgrms (0.65 micromol) of 2 alpha-methyl-9-alpha-fluorocortisol/day subcutaneously. 3. Saline polydipsia occurred with both steroids with both rat strains, though significantly less with the Long-Evans rats. Both types of rats became hypertensive and developed cardiac and renal enlargement with both steroids. Hypertension developed more rapidly with 2 alpha-methyl-9 alpha-fluorocortisol. 4. Thus mineralocorticoid hypertension can be produced in the Charles River Long-Evans rat, and the development of adrenal-regeneration hypertension in this rat strain is not incompatible with a mineralocorticoid etiology for adrenal-regeneration hypertension.
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PMID:Hypertension with mineralocorticoid administration to the Long-Evans rat. 47 92

In our laboratory, chronically feeding cadmium to groups of rats has been reproducibly associated with average increases of 15 to 20 mm Hg in systolic pressure. A total of 497 female Long-Evans rats were continuously provided with drinking water fortified with five essential elements and containing from 0.01 to 50 ppm cadmium, as the acetate, from weaning for as long as 30 months. These rats, plus 311 matched control animals which received fortified water without added cadmium, were fed a special low-cadmium diet. All 808 rats were weighed at least monthly as a screen for cadmium toxicity, and their systolic pressures were measured every 3 or 6 months. The two lowest concentrations of cadmium tested (0.01 and 0.03 ppm) were not pressor; the three highest concentrations (10, 25, and 50 ppm) ultimately proved to be toxic. All indirect systolic pressures (each measured in triplicate) of all rats which received 0.1 to 5 ppm cadmium (i.e., nontoxic pressor doses) averaged 15.0 mm Hg more than simultaneously measured pressures of control rats. This average increase over the control pressure is extremely significant statistically, even though it seems relatively small in absolute terms. Occasionally, however, some rats had much larger than average increases in pressure; thus, 10 of 60 rats receiving from 0.1 to 0.5 ppm cadmium for 18 months had systolic pressures that were more than 50 mm Hg above the average pressure of the control rats. Cadmium-induced hypertension is not limited to females or to a particular strain. Although we have usually used one strain of female Long-Evans rat from a single source, males of the same strain and female Sprague-Dawley rats have also developed comparable hypertension. All subgroup II elements can apparently induce similar increases in systolic pressure averaging 15 to 20 mm Hg, but cadmium is pressor in much smaller amounts than mercury or zinc. Thus, to induce a demonstrable increase in pressure requires more than ten times as much divalent mercuric ion as cadmium and more than 1000 times as much zinc as cadmium. Exposure to another metal along with cadmium can markedly alter the ability of cadmium to induce hypertension. Selenium protects against the hypertension induced by twice as much cadmium. Large excesses of both zinc and copper have also inhibited the induction of hypertension by cadmium. In contrast, lead, which like cadmium, can also induce hypertension, augments rather than inhibits cadmium-induced hypertension; thus, lead and cadmium together can induce an average increase in systolic pressure in excess of 40 mm Hg, at least twice as large as is usually induced by either metal alone.
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PMID:Increase in the systolic pressure of rats chronically fed cadmium. 48 39

In order to investigate the vasopressor role of ADH in the regulation of blood pressure, passive immunization experiments with an antibody to AVP were carried out in experimentally hypertensive rats. In hypertensive rats treated with deoxycorticosterone acetate (DOCA), spontaneously hypertensive rats (SHR) and spontaneously hypertensive stroke-prone rats (SHR-sp), the intravenous injection of a specific vasopressin antibody resulted in a transient fall of blood pressure of 11 approximately 25mmHg, while in rats with two-kidney Goldblatt hypertension and normal rats, the blood pressure was not affected. This strongly suggests that ADH contributed to systemic vaso-constriction in DOCA hypertension and spontaneous hypertension in rats.
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PMID:[The vasopressor role of ADH in the maintenance of blood pressure in experimentally hypertensive rats (author's transl)]. 49 16

The effects of d,l-alpha-tocopheryl nicotinate (EN) on model hypertension in rats were studied in comparison with d,l-alpha-tocopheryl acetate (EA). The progress of hypertension in young SHR during the 9th to 15th weeks after birth was markedly accelerated by replacing their driking water with 1% saline. The highly-developed hypertension in old SHR (9 months of age) was further advanced by salt-loading. Oral administration of 20 or 100 mg/kg of EN or 88 mg/kg of EA, once a day, delayed the progress of hypertension in young SHR and reduced advanced hypertension in old SHR. An antihypertensive effect of tocopheryl esters was also found in DOCA-salt hypertensive rats. The treatment with EN or EA definitely reduced the incidence of pathological changes accompanying model hypertension such as suppressed weight gain, pulmonary edema, myocardial fibrosis, cerebral hemorrhage and protected the animals from death. In antihypertensive effect, EN was about 5 times more active than EA in molecular base, and the effects of EN protecting from pathological changes associated with model hypertension were more definite than those of EA. The treatment with EN or EA reduced water and sodium retention in the DOCA-salt hypertensive animals. This fact may suggest the implication of a mechanism through electrolyte metabolism in the antihypertensive action of these tocopheryl esters.
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PMID:Antihypertensive action of d,l-alpha-tocopheryl nicotinate in rats. 50 48


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