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

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

To evaluate the effect of prostaglandin inhibition on the renal blood flow of the ischemic kidney, we administered indomethacin to 10 anesthetized dogs with renal artery stenosis and contralateral nephrectomy. Following the operation to produce renal ischemia, there was an increase of blood pressure associated with an increase of renin and the prostaglandins F1 (PGF1), and E (PGE). The administration of indomethacin to the intact, normotensive animals caused the anticipated decrease of prostaglandin E, renin, and renal blood flow. However, in the hypertensive dogs, indomethacin caused a paradoxical 45 per cent increase in the renal blood flow, despite a 44 per cent decrease of prostaglandin E. PGF1, PGE, renin, and erythropoietin exhibited the anticipated decreased levels. The study suggests that prostaglandins may not be the sole important factor in the regulation of renal blood flow in the presence of ischemia. Other important factors likely include the renin-sensitive angiotensin, the adrenergic, and the kallikrein-kinin systems.
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PMID:Paradoxical increase of renal blood flow in anesthetized hypertensive dog treated with indomethacin. 48

Hypertension is a frequent complication of reflux nephropathy. The cause of this hypertension is unknown. Our study was undertaken to assess the possible role of the renin-angiotensin system in the hypertension associated with unilateral reflux nephropathy. We selected for study 17 normotensive and 12 hypertensive patients with strictly unilateral reflux nephropathy. There were 3 normotensive and 2 hypertensive patients with a renal vein renin ratio exceeding 1.5. Of these 3 normotensive patients 1 had evidence from divided renal function studies to suggest functional renal ischemia. No consistent evidence was obtained to support the concept that the renin-angiotensin system has a primary role in the non-malignant hypertension of unilateral reflux nephropathy.
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PMID:Renal vein renin concentration in the hypertension of unilateral reflux nephropathy. 67 98

Thirty-three patients with acute pyelonephritis were studied with regard to the changes in plasma renin activity (PRA) along the clinical course of the disease. 1) Abnormally high PRA was found in 64% of patients in the active stage of acute pyelonephritis; they showed a decrease in urinary output of sodium, a reduction in creatinine clearance, and high indices of inflammatory activity. 2) The changes of PRA in the course of acute pyelonephritis were negatively correlated to the urinary sodium excretion and creatinine clearance, but positively to the activity of inflammation, serum sodium concentration and the number of E. coli in the urine. PRA returned to normal with the improvement of pyelonephritis. 3) Concerning the mechanism of hyperreninemia in the active stage of the disease, the following three factors may be considered; renal ischemia, negative sodium balance in the body, and inflammation. Of these, the negative sodium balance seems to be the most important. The patients could not take enough foods to maintain their energy and sodium balance because of fever and pain. 4) The significance of resting PRA in acute pyelonephritis might be to reflect the sodium status in the body, but not to be related to hypertension.
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PMID:Elevated plasma renin activity in patients with acute pyelonephritis. 69 21

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

Renal prostaglandins have several potential functions in renal physiology. Perhaps their best documented role is the maintenance of renal blood flow during renal ischemia, although they are apparently not essential to blood flow autoregulation in the absence of ischemia. Alterations in sodium excretion parallel the hemodynamic changes induced by prostaglandin infusions and prostaglandin inhibition with indomethacin. A direct action on sodium balance is unproven. Numerous studies, in vivo and in vitro, have convincingly demonstrated that prostaglandins or their precursors stimulate renin release and prostaglandin inhibition blunts renin release independent of hemodynamic and electrolyte balance. These functions of prostaglandins have implicated them in the manifestations of Bartter's syndrome, the nephropathy of liver cirrhosis, renovascular hypertension, and other nephropathies.
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PMID:Prostaglandins: renin release and renal function. 72 86

Although the PGs operate mainly in the renal medulla the demonstration of PG biosynthesis in the renal cortex has provided a biochemical basis for a direct relationship between the PGs and the renin-angiotensin system. The formation of PGs is influenced by circulating levels of A I probably by indirect mechanisms. That the release of renin at least under certain experimental conditions is dependent on the PG system is suggested by the following findings: 1. C20:4 increases PRA in the rabbit and rat. 2. Indomethacin decreases PRA in the rabbit. 3. C20:4 stimulates renin release from slices of rabbit kidney cortex. 4. Reduced renal perfusion pressure and ischemia are accompanied by release of both PGs and renin. 5. The release of PG and renin following renal ischemia is blocked by treatment with indomethacin. The actions of the renin-angiotensin system and the renal PGs are, as far as we know them, antagonistic to each other. PGEs are vasodilator, increase renal blood flow, inhibit adrenergic neurotransmission, and cause excretion of electrolytes and water. Conversely, A II is vasoconstrictor, decreases renal blood flow, stimulates adrenergic neurotransmission, and conserves water and electrolytes. Thus, the interaction between the renal PGs and renin seems to be one in which the two hormonal systems stimulate each other's formation or release, but opposes each other's actions. Further studies are necessary to reconcile this apparent contradiction.
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PMID:Interactions between the renal prostaglandins and the renin--angiotensin system. 79 Sep 16

The effect of meclofenamate and indomethacin on renal blood flow and renal vascular resistance was determined under basal experimental conditions and during renal ischemia in pentobarbital-anesthetized dogs. Renal blood flow was measured with an electromagnetic flowmeter and renal arterial pressure was recorded from a catheter in the renal artery. Intra-arterial infusion of indomethacin or meclofenamate in concentrations of 4 and 4 to 8 mu-g/ml, respectively, did not cause any significant change in renal blood flow or renal vascular resistance under basal conditions. During the period of ischemia (50% reduction in renal blood flow), 4 mu-g/ml of either prostaglandin synthetase inhibitor caused a marked increase in renal vascular resistance. Prostaglandin E in the renal venous blood was decreased at the time renal vascular resistance was increased by meclofenamate. The renal vasoconstrictor response to angiotensin II injected intravenously was potentiated by both inhibitors under basal as well as ischemic conditions, which also suggested that prostaglandin synthesis was inhibited. The angiotensin antagonist 1-sar-8-ala-angiotensin II was infused intra-arterially in concentrations of 20 and 40 mmu-g/ml during renal ischemia. Subsequent administration of meclofenamate increased renal vascular resistance only slightly. The results of these experiments indicated that renal prostaglandins have more influence on renal blood flow during renal ischemia than under basal conditions, and that the renin-angiotensin system may be involved in activating synthesis and release of prostaglandins during ischemia.
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PMID:Influence of the renin-angiotensin system on the effect of prostaglandin synthesis inhibitors in the renal vasculature. 80 74

Two cases of renal arterial aneurysm or diffuse renal arterial dilatation are presented. Frequency, pathogenesis, clinical appearance, and prognosis of this disorder are discussed. Major complications include rupture or thrombosis of the renal artery, and hypertension due to renal ischemia; the latter is best diagnosed by renin determination in renal venous blood collected by selective catheterization.
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PMID:[Renal arterial aneurysms--diffuse renal arterial ectasia. (Review and case histories) (author's transl)]. 84 59

The half-life of circulating renin was studied in normal rats and in rats with a single kidney that was ischemic. The resulting disappearance curve represented the sum of two exponentials. The average half-life of the fast component was 11.5 minutes for normal rats, 11 minutes for rats with mild renal ischemia, and 8 minutes for rats with severe renal ischemia. The mean half-life of the slow component was 67 minutes in normality, 84 minutes in mild ischemia, and 121 minutes in severe ischemia. Also, the calculated proportion of the slower component was different for each group--60.3% in normality, 68.2% in mild ischemia, and 82.2% in severe iischemia. The results suggest that more than one kind of renin may be produced and released by the kidney, and also that renal ischemia may modify the normal metabolism of renin.
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PMID:Half-life of circulating renin under different experimental conditions. 87 63


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