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

Observations relating to hypertension in humans and rat experiments have been reviewed from several viewpoints including clinical medicine, pathophysiology, epidemiology, and genetics. It seems likely that much of essential hypertension results from excessive salt intake by individuals with an inherited inability to excrete sodium efficiently which is compensated by blood pressure elevation. A few major genes are likely responsible for a few basic mechanisms involving renal membranes and hormones controlling sodium transport. Excess hypertension in blacks, diabetics, the elderly, and oral contraceptive users can be explained by this theory. If hypertension and other genetically predisposed CHD risk factors are to be fully understood, future studies are needed with detailed data on both genetic and environmental factors, and analytic tools that allow an adequate examination of their interactions.
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PMID:Salt, hypertension, and genetic-environmental interactions. 39 27

1. Salt intake and the incidence of hypertension correlate between populations. 2. Salt intake within a population may correlate with the incidence of hypertension. 3. Disorders that lead to retention of salt cause hypertension. 4. Modest salt restriction reduces blood pressure in many patients. 5. Reducing salt balance and preventing the compensatory rise in angiotensin II controls blood pressure in most patients. 6. Salt is the probable cause of the epidemic of hypertension in the Western world; this could be prevented by salt restriction.
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PMID:The evidence that salt is an important aetiological agent, if not the cause, of hypertension. 39 89

1. The pressor response to angiotensin II was reduced in rats with early (less than 6 weeks) and chronic (greater than 4 months) Goldblatt two-kidney, one-clip hypertension and enhanced in DOCA-salt hypertension. 2. Converting enzyme inhibition with captopril brought the angiotensin pressor response curves into closer proximity although the DOCA hypertensive rats were minimally hyper-responsive and rats with early and chronic renovascular hypertension showed slightly reduced responsiveness. 3. After bilateral nephrectomy the pressor responses to angiotensin were similar. 4. The pressor response to angiotensin II in these animals was inversely related to plasma renin concentration and therefore largely dependent upon receptor occupancy by endogenous angiotensin II. There is no evidence for enhanced pressor responsiveness to angiotensin in either renovascular or DOCA hypertension.
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PMID:Pressor responsiveness to angiotensin in renovascular and steroid hypertension. 39 91

Renin is a hormone secreted by the juxtaglomerular cells of the kidney; it interacts with a plasma protein substrate to produce a decapeptide prohormone angiotensin I. Converting hormone located on vascular endothelium converts the decapeptide to an octapeptide, angiotensin II, which effects vasoconstriction, the secretion of aldosterone by the adrenal cortex, and retention of sodium by the kidney. The biosynthesis and control of renin secretion are not well understood, and the question as to whether renin is synthesized and stored in a larger precursor form is as yet unresolved. Whether or not higher molecular weight or inactive forms of renin in plasma have a role in controlling renin activity or whether they simply represent a degradative pathway for renin is as yet uncertain. The availability of several inhibitors of the renin-angiotensin system has served to define the role of renin both in normal cardiovascular homeostasis and in renovascular hypertension. It appears that renin plays an important role in maintaining blood pressure in the salt- or volume-depleted state and that it is responsible for the initial phases of renovascular hypertension in any model of this disease process. Renin's part in chronic renovascular hypertension depends on whether or not sodium is permitted to accumulate. If sodium intake is restricted or if sodium excretion is unimpaired (such as in two-kidney renovascular hypertension models), renin continues to play a significant role during the chronic phase.
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PMID:The role of renin in the control of the circulation and in hypertensive disease. 39 5

We studied the blood pressure, natriuretic, kaliuretic and humoral responses of 347 normal subjects after volume expansion and volume contraction to examine possible differences among whites, blacks and subjects of different ages. According to outpatient 24-hour urine collections, blacks excreted less sodium and potassium than whites. After similar states of sodium intake were achieved among all subjects, 2 liters normal saline were given i.v. Blacks and subjects greater than or equal to 40 years excreted less sodium than whites or subjects less than 40 years, over a 24-hour period. In addition, blacks excreted less potassium. The delay in sodium excretion occurred during the first 12 hours after the salt load. Blacks had a greater suppression of plasma renin activity than whites 24 hours after saline. Blacks also had higher blood pressures than whites after saline administration; their pressure remained elevated until furosemide was given. Furosemide, 120 mg over 24 hours, evoked greater natriuresis, but less kaliuresis in blacks than in whites. The greater prevalence of hypertension in both blacks and older subjects may be related to relatively blunted natriuretic responses when these groups engage in the high sodium-low potassium intake characteristic of our society.
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PMID:Effects of volume expansion and contraction in normotensive whites, blacks, and subjects of different ages. 42 5

The suggestion that cadmium-induced hypertension in rats might be due to renal sodium retention, known to result from Cd treatment, was examined. Young female rats were given a regimen of intraperitoneal cadmium treatments reported to cause hypertension reliably within a month. They were sensitized to the development of salt hypertension by removal of one kidney and then given 1 percent saline solution to drink. Over a five-week period, experimental animals consistently drank more saline than controls, despite which fewer of them became hypertensive, with the result that the average systolic pressure of controls finally reached the hypertensive range, whereas the experimental group remained normotensive. Cadmium treatment had no detectable effect on growth, the hemogram, serum Na and K, or the weight of liver, kidney, heart, spleen, thymus, or adrenal glands. There was thus no evidence that cadmium caused any adverse constitutional or hemodynamic effects, but it appeared to retard the development of salt hypertension. The results do not support the suggestion that the hypertensive effects of cadmium are modulated by sodium-retaining influences on the kidney.
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PMID:Effect of cadmium on salt hypertension in rats. 42 35

Salt-induced hypertension in Dahl's genetically hypertensive rat has been attributed to humoral or renal factors. However, a recent study from our laboratory suggested that neurogenic mechanisms contribute to salt-induced increased in hindquarters vascular resistance in Dahl salt-sensitive (S) rats. In the present study, we examined the hypothesis that "chemical sympathectomy" with 6-hydroxydopamine (6-OHDA) prevents salt-induced hypertension and increased vascular resistance in S rats. Hypertension did not develop during high-salt diet (8% NaCl) in S rats treated with 6-OHDA, (75--100 mg/kg ip), whereas in rats treated with vehicle, hypertension developed after 4 wk of high salt diet. Chow consumption, sodium excretion, and weight gain were not altered by 6-OHDA. Hindquarters vascular resistance and neurogenic vasoconstrictor tone were significantly lower in S rats treated with 6-OHDA than in S rats treated with vehicle. 6-OHDA also significantly reduced responses to direct sympathetic nerve stimulation and tyramine. These results suggest that an intact sympathetic nervous system plays an essential role in the development of salt-induced increase in blood pressure in Dahl S rats.
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PMID:Prevention of salt-induced hypertension in the Dahl strain by 6-hydroxydopamine. 43 73

Experimental hypertension was produced in nine dogs by continuously infusing isotonic saline after renal mass had been surgically reduced to approximately 30% normal. Data were collected during 8 days of base-line measurements and 13 days of saline infusion to determine the cause of the initial increase in cardiac output observed in this type of hypertension and to measure other variables possibly important in the pathogenesis of hypertension. During the infusion period, these dogs demonstrated an increase in arterial pressure to hypertensive levels, transient increases in blood volume, sodium space, and cardiac output, initially depressed then subsequently elevated total peripheral resistance, and decreases in plasma renin activity and plasma aldosterone concentration. The mean circulatory filling pressure increased 4.7 Torr by day 3 and was still elevated 2 Torr at the end of the 2nd wk of infusion. We conclude that the initial increase in cardiac output in salt-loading hypertension is due to elevated fluid volumes and the associated increase in mean circulatory filling pressure.
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PMID:Essential role of mean circulatory filling pressure in salt-induced hypertension. 43 86

The saralasin test was performed in 68 hypertensives. A clear-cut dependence of the test results on initial plasma-renin concentration and particular sodium balance was demonstrated. Because of this dependence the saralasin test should be performed only under constant conditions. A mild stimulation of the renin-angiotension system by salt restriction to a mean sodium excretion of 50 mmol daily and 80 mg furosemide by mouth 12 hours before the test seems best. In this way essential and renovascular hypertension could be distinguished with considerable reliability (P less than 0.001). Among patients with essential hypertension one could clearly separate those with high plasma-renin concentration from those with a normal or low one. Among patients with renovascular hypertension those with haemodynamically significant renal artery stenosis could with high probability be distinguished from those with non-effective stenosis. A positive saralasin test without testing the function of the normal contralateral kidney does not provide an indication for operation.
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PMID:[The saralasin test in the diagnosis of hypertension (author's transl)]. 43 89

Experimentally induced cerebral aneurysms in rats treated with unilateral ligation of the common carotid artery, deoxycorticosterone and salt hypertension, and beta-aminopropionitrile, were studied macroscopically and with light-microscopy. The material consisted of 13 aneurysms located on the anterior cerebral-anterior communicating arterial complex and one on the posterior cerebral artery. The findings were generally in accordance with that of spontaneous lesions in man. The results show the validity of these experimental aneurysms as a model for saccular cerebral aneurysms in man.
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PMID:Experimentally induced cerebral aneurysms in rats: Part III. Pathology. 44 17


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