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Query: UMLS:C0920646 (renal ischemia)
 2,515 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Relative renal ischemia, produced by a variety of interventions, is modulated or buffered by prostaglandins synthesized within the kidney. These prostaglandins, however, do not account for renal autoregulation in its classic sense. They can facilitate salt and water excretion, largely through effects on physical forces in proximal peritubular capillaries, as evidenced by augmented renal blood flow. Renal prostaglandins may play a role in chronic water balance, but they probably are not important in chronic electrolyte homeostasis. There are several potential mechanisms by which renal prostaglandins could exert antihypertensive efects. Establishment of the importance of these agents, however, as antihypertensive hormones remains a challenge for future investigation.
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PMID:Renal prostaglandins. 23 76

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

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

The biochemical processes which transform baroreceptor, beta-adrenergic and macula densa signals into an increase or a decrease of renin secretion are unknown. Evidence is presented that the renal PG system is intimately involved in the mechanisms regulating the release of renin. In vivo stimulation of renal PG synthesis by arachidonic acid (C20:4) or furosemide increases renin release. PG synthesis inhibitors decrease basal renin release and reduce the renin release following stimulation with C20:4, furosemide and renal ischemia. In vitro, C20:4 and the PG-endoperoxides stimulate renin release from the rabbit kidney cortex whereas PGF2alpha inhibits it. This suggests an intrinsic role in the renin release mechanism of PGs, synthesized at or near the juxtaglomerular apparatus. The operation of this PG effect on renin release may depend upon a salt intake related control of PG synthesis and of conversion of PGE2 to PGF2alpha. Increased or decreased renal PG synthesis may also be the primary event leading to elevated or reduced renin levels in some clinical disorders. In Bartter's syndrome, the elevated renin levels may result from an increase in PG synthesis or a decrease of PGF2alpha formation. In benign, uncomplicated essential hypertension, decreased renal PG synthesis or increased PGS2alpha formation may be the primary mechanism which reduces renin release and renal blood flow.
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PMID:Renal prostaglandins in the control of renin. 69 7

Information defining the renin-angiotensin-aldosterone axis as a control system concurrently regulating salt balance and blood pressure has been applied to examine the role of renin in the causation of experimental and clinical forms of renovascular and renal hypertension and thence to develop criteria for differentiating these entities. Experimantally there are two models of renovascular hypertension, one 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 switches to a vasoconstrictor form, illustrating how the two factors coordinate to maintain blood pressure. Human renovascular and renal hypertensions appear to be sustained by the same two mechanisms. Experimental and clinical studies both indicate that curable renal hypertension is in fact a 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 referenced against sodium excretion. (2) Lacteralization of renin secretion with contralateral suppression rules out occult bilateral disease. It is indicated by V-A = 0 from the uninvolved kidney. (3) A third criterion, (V-A)/A greater than 48 per cent from the ipsilat-eral kidney, identifies renal ischemia. These three criteria, when taken together in a combined scoring analysis, provide high precision in identifying the patient with the vasoconstrictor form of renal hypertension that is potentially reversible by appropriate surgery. Absence of these criteria identifies hypertension associated with either occult or overt bilateral renal disease. In these patients, the volume factor often predominates and is expressed by some suppression of plasma renin levels. Here, removal of renal tissue is contraindicated. Corroborative evidence to support these three criteria can be developed from the blood pressure response to angiotensin blocking drugs or to anti-renin therapy with propranolol. Thus in all of these renal hypertensions, the vasoconstrictor and volume factors can be identified using renin measurements and pharmacologic interventions.
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PMID:New concepts of the renin system and of vasoconstriction-volume mechanisms. Diagnosis and treatment of renovascular and renal hypertensions. 109 53

It is apparent that the split function study and renal vein renin determination are complementary and afford valuable information for selecting patients with potentially curable renovascular hypertension. The split function study, when interpreted with the recently defined split function ratio, offers the clinician a highly accurate means of diagnosing significant renal ischemia. Because the split function ratio shows the disparity between the ischemic and contralateral kidney to a greater degree, the chance of misdiagnosis due to laboratory or physician error is minimized. The split function study, however, is of limited value in patients with pyelonephritis since the water- and salt-losing characteristics of the pyelonephritic kidney may mask significant renal ischemia. In these patients, as well as those with a nonfunctioning kidney or hydronephrosis, the renal vein renin determination is the test of choice. In addition, the added morbidity of the split function study is not warranted in a patient with an elevated peripheral renin which, for interpretation, requires an accurate 24 hour urine for sodium, a renal vein renin ratio outside the range of patients with essential hypertension (renal vein renin ratio greater than 1.7) and evidence of suppression of renin secretion from the contralateral kidney. If, however, the renin determination does not afford convincing evidence of significant renal ischemia in a patient with radiographic evidence of renal arterial stenosis, a split function ratio definitely should be determined to more completely define the pathology. The attendant morbidity of a carefully performed split renal function study does not approach the morbidity and mortality associated with unnecessary surgery or inadequately treated hypertension.
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PMID:Ureteral catheterization studies. 115 55

Renal effects of 1,4-dihydropyridine (DHP)-type calcium antagonists (nitrendipine and nisoldipine) were analyzed in diverse conditions, such as long-term antihypertensive treatment, acute saline-loading, and acute renal failure in rats. In spontaneously hypertensive rats (SHR), 60-week treatment with nitrendipine resulted in normotensive blood pressure values without increasing body weight, an indicator of salt-water retention, or increasing plasma renin activity and plasma aldosterone concentration compared with the untreated rats. After acute saline-loading of normotensive or hypertensive rats, administration of calcium antagonists nitrendipine and nisoldipine increased urinary volume and sodium excretion. This was in contrast to the effects observed with the vasodilator minoxidil, with which salt-water retention was shown. In acute renal failure induced by 60-min renal ischemia in uninephrectomized rats, administration of nisoldipine decreased mortality rate and improved kidney function. The increase in renal tissue calcium content and the decrease in ATP content associated with the renal failure was abolished by nisoldipine treatment. In conclusion, renal protective effects are present with DHP-type calcium antagonists; however, mechanisms in situations such as hypertension or acute renal failure might be different and deserve further analysis.
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PMID:Renal effects of 1,4-dihydropyridines in animal models of hypertension and renal failure. 244 Nov 91

The renovascular hypertension in the Wistar rats was induced by clipping both renal arteries. Within 3-4 weeks arterial pressure (AP) increased to maximal values. According to AP, the rats were divided into two groups: with AP less than or equal to 170 mm Hg and greater than 170 mm Hg. In 5-6 or 10-11 weeks the animals were decapitated and the Na,K-ATPase activities in the wholesome erythrocytes, their ghosts, and the cortex and medulla of kidneys were studied. Changes of the enzyme activity were only found in the medulla. A decreased enzyme activity (-20%) was revealed in the rats with AP less than or equal to 170 mm Hg within 5-6 weeks after renal ischemia, the activity increasing again in 10-11 weeks after the operation. The decreasing of Na,K-ATPase activity within 5-6 weeks after renal ischemia could be a mechanism of adaptation of the salt-water balance in animals.
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PMID:[Effect of bilateral renal ischemia on the sodium, potassium ATPase activity of the kidneys and erythrocytes in rats]. 254 69

Water-electrolyte balance, plasma renin activity and urinary catecholamine excretion were studied for a period of 10 weeks after clipping the renal artery in the rat. Two groups of rats were examined; in Group I, a silver clip was applied on the left renal artery leaving the contralateral kidney untouched; in Group II, both renal arteries were clipped. Neither water-salt retention nor the increase inthe activity of the renin-angiotensin system or in the neural tone seem to be essential in the development of high arterial pressure after renal ischemia. All these factors would seem to be secondary mechanisms the contribution of which would depend on the experimental model or the hypertensive period under consideration.
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PMID:Water-salt balance, plasma renin activity and catecholamine excretion in renovascular hypertension in the rat. 616 29

To elucidate the significance of hypertension associated with cerebrovascular lesions (CVL), renal perfusion pressure (RPP) was controlled by aortic clips of two different sizes in stroke-prone spontaneously hypertensive rats kept under normal or salt-loaded conditions. Tail and femoral arterial pressures (RPPs) in the mildly and severely clamped animals were reduced in proportion to the severity of the clamping. In contrast, carotid pressures in both clamped groups were significantly higher than that in the controls. Proteinuria and hyperreninemia accompanied by arteriolar changes in the renal cortex were observed in the controls prior to the onset of CVL. The renal changes were inhibited by both types of clamping. The onset of CVL was delayed by the mild clamping in salt-loaded animals, but accelerated by the severe clamping in both the normal and salt-loaded animals. Renal cortical blood flow was decreased only by the severe clamping. The results suggest that reduction in RPP and/or renal ischemia, which seems to be due to the hypertensive arteriolar changes in the renal cortex, may be related to the pathogenesis of CVL in the stroke-prone rats with or without hyperreninemia.
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PMID:Implication of renal perfusion pressure in stroke of spontaneously hypertensive rats. 736 76


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