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

The number of lipid droplets of the renal medullary interstitial cells was registered in 40 rats with "two-kidney Goldblatt hypertension" and in 27 sham operated normotensive controls. A strong degranulation in the unclaimed kidneys was always associated with the malignant course of hypertension, characterized by a disturbance in the sodium and water balance. Giving 2 per cent saline in addition to demineralized water as a drinking fluid the decrease in the number of granules was prevented in most of the malignant cases. Significant changes in the granule count were never registered at a benign course of hypertension. Degranulation of the medullary interstitial cells in the unclamped kidneys does not unequivocally represent the loss of medullary antihypertensive function. It seems to be directly determined by the disturbance of sodium and water balance and indirectly by the hypertension.
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PMID:On the lipid granularity of renomedullary interstitial cells in benign and malignant courses of renal hypertension. 47 21

Exposure of rats to cadmium causes a marked depletion of iron in liver and kidney. Selenium neither counteracts or intensifies the influence of cadmium on tissue iron levels. Selenium injections protect against cadmium-induced testicular damage but cause this element to accumulate in the testes at higher concentration than in animals exposed to cadmium without selenium. Selenium injection diverts the binding of cadmium from low molecular weight proteins to high molecular weight ones. Dosing rats with selenium and cadmium or inclusion of Se or Cd in the diet did not result in altered cadmium binding in tissues, raising some questions concerning the environmental significance of these injection experiments. Addition of selenium to a diet containing cadmium decreased the accumulation of cadmium in liver and kidney, but increased its deposition in testes. The metabolism of cadmium bound to metallothionein was markedly different as compared to the inorganic salt of this element. Dietary ascorbate, but not citrate or cysteine, decreased the deposition of cadmium in rat tissues. In some low-level exposure experiments with cadmium (1 to 1000 ppb), no differences were found in the percentage of dose absorbed or rate of cadmium accumulation when provided in food versus water. Female rats tended to absorb more cadmium than males. The binding of cadmium to cytosolic proteins was found to be different between rats fed low levels of cadmium (up to 1 ppm) as compared to those fed high levels of this element (100 ppm). Cadmium was not found to contribute to hypertension in rats, and a summary of results by various investigators is presented. Blood and hair cadmium levels in Oregon residents were found to be highest in employees of a mine, and hair cadmium was found to be respectively higher in smokers than nonsmokers and in metal workers than office workers. No relationships were observed in humans between blood or hair cadmium levels and blood pressure.
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PMID:Cadmium effects in rats on tissue iron, selenium, and blood pressure; blood and hair cadmium in some oregon residents. 48 28

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

This study was undertaken to explore the effects of chronic low-level cadmium ingestion in Dahl hypertension-resistant (R) and hypertension-sensitive (S) lines of rats. Groups of weanling female R and S rats were given 0 or 1 mg cadmium/1. in drinking water and fed either a low salt (0.4% NaCl) or a high salt (4% NaCl) diet for 28 weeks. Cadmium produced hypertension associated with gross cardiac hypertrophy and mild to moderate renal vascular changes in S, but not in R, rats on a low salt diet. Cadmium enhanced the rate and degree of development of salt-induced hypertension without exacerbating the hypercholesterolemia or renal vascular lesions normally observed in S rats on a high salt diet. Cadmium lowered circulating cholesterol levels in both lines on a low salt diet. Cadmium had no influence on growth, blood urea nitrogen concentration, plasma renin activity, tumor formation, or survivorship in R and S rats on either salt diet. This study indicates that the genetic composition is a critical determinant of the adverse effects of chronic low-level cadmium ingestion in rats. In addition to the experimental implications, these findings may have relevance to the problem of human "essential" hypertension.
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PMID:Effects of cadmium ingestion in rats with opposite genetic predisposition to hypertension. 48 40

The importance of salt and water in the pathophysiology of the hypertensive state is well recognized. The current study is the first to report simultaneous measurements of red blood cell mass, plasma volume, extracellular fluid and total body water levels. Studies were performed in 82 white men, 14 with normal blood pressure and 16 with low renin and 52 with normal renin hypertension. The results indicate that subjects with normal renin hypertension compared with age-matched controls are characterized by an absolute increase (1.5 liter/m2) in intracellular fluid (total body water minus extracellular fluid). Furthermore, the ratio of extracellular fluid to total body water is decreased (0.43 to 0.38). No volume differences were found between subjects with low renin hypertension and age-matched subjects with normal renin hypertension. We conclude that subjects with normal renin hypertension compared with age-matched peers are characterized by an expanded intracellular fluid and that subjects with low renin hypertension do not exhibit a unique volume disorder.
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PMID:Volume studies in men with mild to moderate hypertension. 49 11

The effects of continuous intrarenal prostaglandin E2 (PGE2) infusion (7 days) on sodium and water balance, plasma renin activity (PRA), and sodium and water balance, plasma renin activity (PRA), and mean arterial pressure (MAP) were examined in conscious, unilaterally nephrectomized dogs maintained on a fixed sodium intake of 55 meq/day. PGE2 infusion (2 microgram/min) resulted in a sustained threefold increase in both urine output and water intake without a measurable change in glomerular filtration rate. PRA increased from 0.4 +/- 0.1 during the control period to 2.2 +/- 0.9 ng AI.ml-1.h-1 on day 1 and averaged 3.6 +/- 0.5 for the remaining 6 days of PGE2 infusion. Concurrently, MAP increased from 102 +/- 3 to a maximum of 117 +/- 4 mmHg on day 5; changes in PRA and MAP were significantly correlated (r = 0.96, P less than 0.001). Sodium excretion increased from 54.5 +/- 3 to 88.0 +/- 19 meq/day on day 1, and then declined to an average of 64.8 +/- 1 meq/day for the remaining 6 days of infusion. All variables returned to the control level during the recovery period. Intravenous infusion of PGE2 (2 microgram/min) yielded directionally similar but statistically insignificant effects. It is concluded that chronic intrarenal PGE2 infusion results in marked diuresis, polydipsia, a moderate loss of sodium, enhanced PRA, and mild hypertension.
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PMID:Prostaglandin E2-induced hypertension in conscious dogs. 49 30

The role of central nervous system (CNS) catecholamines in the development of hypertension and the control of drinking behavior was assessed in rats by depleting these amines with 6-hydroxydopamine (6-OHDA). Intraventricular administration of 6-OHDA completely prevented the development of one-kidney renal hypertension and abolished the associated increase in water consumption. 6-OHDA-treated rats showed deficits in drinking behavior when challenged with subcutaneous injections of angiotensin II (AII) and hypertonic sodium chloride. The acute pressor responses produced by intraventricular injections of AII and carbachol were virtually abolished by central catecholamine depletion. However, drinking produced by central cholinergic stimulation remained intact while AII drinking was significantly reduced. These data demonstrate that the integrity of CNS catecholamines is required for the development of one-kidney renal hypertension and the increased drinking which accompanies it. In addition, destruction of central catecholamine-containing neurons allows for a specific dissociation of the pressor and drinking responses produced by central cholinergic but not AII stimulation.
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PMID:Role of central catecholamines in the control of blood pressure and drinking behavior. 49 58

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

Subtotal nephrectomy was produced in male Wistar rats and the evolution of arterial pressure, water distribution and electrolytic composition of muscle and arterial tissue were studied. Also, the modifications produced by a chronic administration of saline load were evaluated. The incidence of hypertension is higher in the group that received saline load but the levels of the blood pressure were similar in both groups of hypertensive animals. The total water is increased in all the groups, except at the fourth week in the animals that did not receive saline load, in which it was decreased. The extracellular space is augmented in all groups and the plasma volume increased in the early phases of the experimental period with exception of the normotensive rats without saline load. No alterations were observed in the electrolytic muscle content, and the total water and potassium and chloride content of the arterial tissues was increased without modifications in the sodium content. The possible relationship of these alterations with the development of hypertension are discussed.
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PMID:Body fluid changes in hypertensive rats. Their modifications by saline load. 50 66

Numerous community drinking water sources have elevated levels of both sodium and lead. Recently reported studies have indicated that elevated levels of sodium in drinking water may be a facter in the development of elevated blood pressure. The question of how elevated levels of lead may affect sodium induced elevated blood pressure is addressed. The hypothesis is developed which states that elevated levels of lead exposure will not interact with sodium to enhance the development of renin angiotensin aldosterone related hypertension but in fact may even diminish the effects of exposure to elevated amounts of sodium on blood pressure through a depression of plasma renin activity.
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PMID:Does exposure to elevated levels of lead enhance sodium induced hypertension? 51 19


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