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

The increase of the content of triphosphoinositide in the erythrocyte membrane in rats with spontaneous and renal hypertension and decrease of phosphatidylinositol at spontaneous hypertension were revealed.
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PMID:Phosphoinositide content in the erythrocyte membrane of rats with spontaneous and renal hypertension. 20 58

1 Prolonged infusion (11 h) of both saralasin and angiotensin-converting enzyme inhibitor (SQ20881) gradually lowered BP in two-kidney hypertensive rats to levels similar to that in normotensive rats infused with dextrose. 2 Saralasin did not lower BP in DOCA-salt hypertensive rats. 3 These observations support the notion that in chronic renal hypertension, angiotensin II may maintain hypertension by a slowly developing action. 4 Plasma angiotensin II in rats infused with SQ20881 was suppressed relative to renin, but was not eliminated. 5 Chromatography of angiotensin II extracts from dogs infused with converting enzyme inhibitor (SQ14,225) showed that the very high levels of angiotensin I achieved after treatment with SQ14,225 can lead to falsely high estimated angiotensin II levels as a result of angiotensin I cross-reacting with the angiotensin II assay.
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PMID:Inhibitors of the renin-angiotensin system in experimental hypertension, with a note on the measurement of angiotensin I, II and III during infusion of converting-enzyme inhibitor. 22 15

Information defining the renin-angiotension-aldosterone axis as a control system concurrently regulating salt balance and blood pressure has been applied to reexamine the role of renin in experimental and clinical forms of renovascular and renal hypertension, and thence to develop criteria for differentiating these entities. Experimentally, there are two models of renovascular hypertension; one is characterized by excess renin with reduced sodium (vasoconstrictor form) and the other by excess sodium with reduced renin (volume form). But with sodium depletion, the volume form converts to a vasoconstrictor form illustrating how the two factors coordinate to maintain blood pressure. In man, renovascular and renal hypertensions appear to be sustained by the same two mechanisms. Studies in man show that, in the absence of unilateral disease, the supine renal venous renin level in each kidney is consistently 24 percent higher than the peripheral level. Because of this constant relationship, the peripheral renin level is a measure of the renal secretion rate. Our studies indicate the curable unilateral renovascular hypertension is, in fact, renin-dependent vasoconstrictor hypertension. Three criteria, derived from four renin measurements, identify this situation: (1) Hypersecretion of renin is reflected by a high peripheral level when indexed against sodium excretion. (2) Lateralization of renin secretion with contralateral suppression rules out occult bilateral disease. It is indicated by V-A equal 0 from the uninvolved kidney. (3) (V-A)/A greater than 48 per cent from the ipsilateral kidney supports unilateralization. With data derived from patients with essential hypertension as a reference, the degree to which (V-A)/A is greater than 0.48 can be used to estimate the degree of renal ischemia, using Fick's principle. Corroborative evidence to support these three criteria can be developed from the blood pressure response to angiotensin blocking drugs or to antirenin therapy with propranolol. Clinical analysis validates these criteria to identify curable hypertension from unilateral renovascular or parenchymal disease. In patients with either occult or overt bilateral renal disease, the volume factor often predominates and is expressed by some suppression of plasma renin levels. Continued
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PMID:The renin axis and vasoconstriction volume analysis for understanding and treating renovascular and renal hypertension. 23 77

The effect of arterial hypertension on cerebral blood flow was studied by the intracarotid 133Xe clearance method in baboons. The arterial blood pressure was raised in gradual steps with angiotensin. Baboons with renal hypertension of 8-12 weeks duration were studied along with normotensive baboons. In initially normotensive baboons, cerebral blood flow remained constant until the mean arterial blood pressure had risen to the range of 140 to 154 mm Hg; thereafter cerebral blood flow increased with each rise in mean arterial blood pressure. In the chronically hypertensive baboons, cerebral blood flow remained constant until the mean arterial blood pressure had been elevated to the range of 155 to 169 mm Hg. Thus, in chronic hypertension it appears that there are adaptive changes in the cerebral circulation which may help to protect the brain from further increases in arterial blood pressure.
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PMID:Upper limit of cerebral blood flow autoregulation in experimental renovascular hypertension in the baboon. 23 55

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

In a nineteen-year-old male in whom severe and protracted hypertension developed after a successful renal transplantation, the removal of the diseased kidneys resulted in restoration of normal blood pressure. Prenephrectomy blood samples obtained from the venous drainage of all three renal veins demonstrated no evidence for excessive renin secretion, nor was a significant difference in renin activity found between any two kidneys. It is postulated that the patient may be a clinical variant of the experimental form of renal hypertension with normoreninemia. Alternatively, the remnant kidneys may be implicated to produce a nonrenin pressor substance.
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PMID:Post-transplant hypertension. Normoreninemic severe hypertension treated by bilateral nephrectomies. 32 86

The complex hormonal action of angiotensin II in the long-term control of blood pressure or sodium metabolism, or in renal hypertension, is not completely understood. Structure-activity relations with analogues of angiotensin II gave information about the functions responsible for pressor and myotropic response in the molecule that led to the synthesis of competitive antagonists of this hormone. These antagonists, however, show variable agonist/antagonist ratios in different species or different tissues of the same species. This fact necessitates further work to induce tissue specificity. Although des-Asp1-angiotensin II ("angiotensin III") has been recognized as a hormone, its exact role in the biosynthesis of aldosterone is yet to be discovered. The antagonists such as des-Asp1-[Ile8]-angiotensin II or des-Asp1-[Thr8]-angiotensin II have provided important leads in this direction. Many of the biologic effects of angiotensin I have been attributed to its conversion to angiotensin II by the converting enzyme. Recent investigations indicate that angiotensin I itself may play a direct role; however, most of these studies were carried out by inhibiting the converting enzyme activity with peptides obtained from the venom of Bothrops jararaca. Since these peptides also potentiate bradykinin action, the observed biologic activities could be caused by either angiotensin I or bradykinin. Bsides, converting enzyme is no longer thought to be a single enzyme and its nature varies from species to species and from tissue to tissue in the same species. Renin inhibitors related to renin substrate or pepstatin are not freely soluble in plasma and are not effective under physiologic conditions. This points to the importance of renin inhibitors isolated from kidney or other natural sources. Thus, although the renin-angiotensin system appears to be an integral part of the problem of hypertension, characterization of various converting enzymes, roles of extrarenal renin, isorenin, tonin, and brain-renin, and the involvement of other humoral, neurogenic, and immunogenic factors should be pieced together to get a clear picture of the hypertension problem.
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PMID:Pathogenic factors involved in renovascular hypertension. State of the art. 32 61

The influence of intravenous injection of Prostacyclin (PGI2) on systemic blood pressure was investigated in conscious and anaesthetized hypertensive rats. PGI2 in doses of 1.0, 5.0 and 10.0 micrograms/kg showed a dose dependent antihypertensive effect in conscious rats with spontaneous and chronic renal hypertension. A similar response could be demonstrated in conscious rats with normal blood pressure with doses of 1.0, 10.0 and 100.0 micrograms/kg. In anaesthetized rats with acute renal hypertension or blood pressure increase, induced by continous infusion of Angiotensin II or Norepinephrine, PGI2 caused a marked decrease of blood pressure. PGI2 induced an increase of plasma renin activity in anaesthetized rats with doses of 0.1, 1.0 and 10.0 micrograms/kg. These findings support the suggestion of an antihypertensive role for PGI2 in experimental hypertension.
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PMID:Antihypertensive effect of prostacyclin (PGI2) in experimental hypertension and its influence on plasma renin activity in rats. 36 7

Renal hypertension is better understood now as a result of the development of new laboratory techniques which permit the identification of the surgically curable forms of renovascular and renal parenchymal hypertension. The rationale for and efficacy of these new advances are discussed and a practical approach to the diagnosis of renal hypertension is offered.
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PMID:Laboratory tests in the evaluation of renal hypertension. 38 89

The convoluted proximal and straight distal tubules and the medullary collecting ducts in kidneys of rats with ischaemic renal hypertension and with genetic spontaneous hypertension were studied by means of electron microscopic morphometry. The volume of mitochondria, the area of their cristae, of the outer surface and of membranes of the intercellular labyrinth, and other ultrastructural characterisitcs were calculated. No significant differences were found in proximal tubules between experimental and control animals, although in the distal tubules in both experiments the coefficient characterizing the level of morphologic organization of mitochondria, which takes into account their basic morphometric parameters, was reduced in hypertensive animals as compared with the intact ones. The volume of mitochondria and the area of their cristae in collecting ducts, and also the area of membranes of the intercellular labyrinth were increased. Our results suggest that in hypertension the reabsorption of substances from the proximal tubules is essentially normal, that it is reduced at the beginning of the distal tubules but is intensified in the collecting ducts.
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PMID:Morphometric study of the ultrastructure of nephrons and collecting tubules in the kidney of rats with renal and spontaneous hypertension. 41 29


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