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

1. Variables involved in the genesis of hypertension in male broad-breasted white turkeys include social environment, obesity and high salt intake. 2. The hypertension is characterized by low plasma renin activity and, with increasing age, normal to high plasma aldosterone. 3. Medionecrosis of the abdominal aorta is a common pathological finding. 4. The absence of atherosclerotic plaques is probably related to the high concentrations of alpha-lipoproteins.
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PMID:The natural history of hypertension in turkeys. 28 53

1. The pressor responses to hypertonic saline and angiotensin II introduced into the left lateral ventricle were both significantly greater in salt-sensitive (S) rats compared with salt-resistant (R) rats, with all rats on a low Na diet. 2. When S rats were given thiazide to nullify the pressor effect of dietary NaCl, their blood pressure averaged only 5 mmHg higher than that of the R rats; nevertheless, these S rats had significantly higher central nervous system pressor responses to angiotensin II and hypertonic saline. 3. Thus, if excessive dietary Na increases blood pressure by way of action on the central nervous system, these heightened pressor responses could partially account for the NaCl hypertension in S rats. Alternatively, depressed central nervous system pressor responses in R rats could partially explain the resistance of R rats to NaCl hypertension.
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PMID:Central nervous system pressor responses in rats susceptible and resistant to sodium chloride hypertension. 28 56

1. Aorta homogenate contains renin-like activity which on incubation generates angiotensin I over a wide pH range. 2. Rat aortic renin measured at an incubation pH of 6.5 rose and fell in parallel to plasma renin with salt depletion and salt-loading respectively. Renin little relationship with plasma renin. 3. Aortic renin (pH 6.5) was elevated in Goldblatt-two kidney hypertension and slowly fell for 24h after bilateral nephrectomy whereas the fall in plasma renin was complete by the first hour. Aortic renin (pH 5.3) was also high, but did not fall after bilateral nephrectomy. 4. Aortic renin (pH 6.5) is probably derived from plasma renin whereas renin measured at pH 5.3 is probably a tissue renin. 5. The prolonged half-life of aortic renin (pH 6.5) explains the observation that the renin-angiotensin system appears to be active in maintaining blood pressure for several hours after bilateral nephrectomy whereas the decline in plasma renin is rapid and does not continue significantly beyond 1 h.
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PMID:Role of persistent vascular renin after bilateral nephrectomy in Goldblatt-two kidney hypertension. 28 58

The role of brain catecholaminergic neurones in the pathogenesis of DOCA-salt hypertension in the rat was investigated by selective depletion of central catecholamines using intraventricular or intracisternal administration of 6-hydroxydopamine (6-OHDA). Only the intraventricular injections prevented the development of hypertension. In addition, intraventricular 6-OHDA reversed the hypertension produced by two weeks but not six weeks of DOCA-salt treatment. The ability of intraventricular injections of 6-OHDA to prevent or reverse DOCA-salt hypertension while intracisternal injections do not, appears to be related to the greater depletion of brain catecholamines produced by the intraventricular injections. Only in the spinal cord and in the locus coeruleus were the norepinephrine contents depleted equally by either injection route. These findings suggest that central catecholaminergic neurones other than those originating in the locus coeruleus or descending in the spinal cord are important in the initiation, but not in the long term maintenance, of DOCA-salt hypertension. The influence of the central catecholamine neurons involved in the development of DOCA-salt hypertension might be mediated neurally via nonadrenergic pathways or hormonally via the brain-pituitary-endocrine system.
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PMID:6-hydroxydopamine destruction of central adrenergic neurones prevents or reverses developing DOCA-salt hypertension in rats. 32 22

Studies on the Kyoto (SHR) and the New Zealand (GHR) strains of genetically predisposed hypertensive rats have shown that in the SHR neurogenic influences, primarily of higher central origin, play an important role in the initiation of hypertension. Studies on human essential hypertension indicate that this may also be true for man, although it is far from being the sole explanation. Brookhaven hypertension-prone rats illustrate the interaction between genetic and exogenous factors since they require an overload of salt for the development of high blood pressure. The Milan hypertensive rats (MHS), on the other hand, illustrate a genetic deviation of renal function with imbalance between glomerular filtration and tubular resorption of sodium and water, which may simulate at least some variants of the relatively mild forms of low renin hypertension in man. Structural adaptive vascular changes have been demonstrated in SHR and GHR and in nongenetic renal hypertension in rats, and there are several indications of their presence in MHS. Thus, regardless of the nature of the initiating factors, these secondary but rapidly established changes occur and greatly contribute to the maintenance and acceleration of the hypertensive state. The vascular changes can even be regarded as a common denominator for chronic hypertension and serve as an element which, in fact, reinforces the initiating mechanisms. The progress of the vascular changes can be interfered with by reducing the pressure load. Lowering the blood pressure by pharmacologic treatment is most effective when the treatment is initiated as such an early age when the cardiovascular structural adaptation is still minimal. Treatment in later phases is less successful since the adaptive increases in cardiac and vessel wall thickness can then no longer be fully normalized by pressure reduction because of increased amounts of collagen and other connective tissue elements in the vessel wall, which regress poorly. An increased wall thickness of the resistance vessels implies a vascular hyperreactivity to constricting influences which, in turn, rapidly brings the blood pressure back to supranormal levels as soon as therapy is stopped.
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PMID:Mechanisms of spontaneous hypertension in rats. 32

Partial infarction of one kidney and contralateral nephrectomy was followed by a similar initial increase in blood pressure in athymic (nude) and normal mice of the C57/BL/6J strain. The chronic phase of the hypertension was, however, thymus dependent, since the athymic mice failed to maintain an increased blood pressure, in contrast to the normal mice. A response of thymus transplantation in athymic mice was the ability to maintain the blood pressure high in the chronic phase of the hypertension, whereas cyclophosphamide treatment to the normal hypertensive mice decreased the blood pressure in the chronic phase of the hypertension, but not in the early (acute) phase. Some perivascular round cell infiltrations were found in the uninfarcted part of the kidney in normal and thymus-transplanted nude mice after 80 days of hypertension, but the degree of cellular reaction was less than previously observed in the NMRI-strain of mice. Substantial perivascular cellular infiltrations, which appeared to be thymus-dependent, occurred in the ischemic border-zone of the infarcted area. Athymic mice of the NMRI-strain were able to develop the initial blood pressure elevation of DOCA/salt hypertension during the chronic phase of loomis hypertension, in which phase the arterial pressure otherwise would be declining towards normal values.
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PMID:The importance of thymus in the pathogenesis of the chronic phase of hypertension in mice following partial infarction of the kidney. 33 61

Saralasin, a specific competitive inhibitor of angiotensin II, was administered in a controlled, prospective study designed to test the hypothesis that this agent is a useful tool for the detection of renovascular hypertension. 13 patients, 11 with renovascular hypertension and 2 with high-renin essential hypertension, showed a gross, readily apparent decrease in blood pressure after receiving saralasin. 8 patients with essential hypertension and normal or low renin levels exhibited no depressor response to the drug. In the patients with renovascular hypertension, blood pressure response during angiotensin blockade compared favourably with renal vein renin determinations as a predictor of operative results. Because saralasin testing has resulted in few if any falsely positive or negative results when considered as a diagnostic procedure for renin-mediated hypertension, and because it is safe, it may become an ideal initial screening procedure. The saralasin test (either bolus injection or sustained infusion) is completely valid only if the patient is mildly salt-depleted, is not taking other antihypertensive medication, and is genuinely hypertensive at the time of the test.
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PMID:Angiotensin blockade in renovascular hypertension: a controlled, prospective study. 33 16

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

Since the anatomical descriptions of Bowman showing differences between nephrons originating in the superficial and deep cortex, the concept of heterogeneity has been extended from identification of dissimilarities between nephrons to recognition of inhomogeneity within major portions of individual nephrons. We are now aware of functional correlates for the anatomical differences between nephrons, between analogous parts of different nephrons, and between the three portions of the proximal tubule and the three or more parts of the distal tubule. The implications of all of these differences for major renal processes, such as isosmotic fluid transport, salt balance, hypertension, urinary acidification, and the concentration or urine are now being defined. It seems likely that new conceptual and technical approaches, especially electron probe microanalysis, will add appreciably to defining the role of heterogeneity in these and other processes. Despite the increasing complexity of nephron heterogeneity, it is recommended that our basic nomenclature be retained and that new findings be incorporated into the schema set forth by Karl Peter. It would be very helpful if reports of investigations on single nephrons or segments of nephrons were to include diagrams delineating the structures on which the work was performed.
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PMID:Structural and functional heterogeneity of mammalian nephrons. 33 47

Approximately 1% of pregnancies are complicated by essential hypertension. During pregnancy the blood pressure often stabilizes or improves. In patients with sustained hypertension, prospective controlled studies have demonstrated enhanced fetal survival when the blood pressure was controlled with antihypertensive medication. Such medication must be chosen carefully to avoid fetal and mateerial toxicity, and diuretics and salt restriction during pregnancy should be avoided. Among patients with essential hypertension the problem accelerates late in pregnancy in 2% to 11%; the acceleration may be predicted by determination of maternal mean arterial pressures and intravascular volumes early in pregnancy. The treatment of accelerated hypertension is identical to that of severe pre-eclampsia. Fetal loss is considerable but can be lessened by careful fetal and maternal monitoring and early controlled delivery. The risks of pregnancy in most patients with essential hypertension are small, and essential hypertension is not a uniform contraindication to pregnancy.
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PMID:Essential hypertension and pregnancy. 34 89


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