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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

It is commonly assumed that the decrease in the effective circulatory volume (ECV) is the major event in acute renal failure (ARF) and the preferential ischemia of the cortex another major modification. Frusemide has been given to try to prevent this change in glycerol-induced ARF because of its effect in redistributing renal blood flow from medulla to cortex. Isontonic saline was also tried to avoid the ECV depletion. The pretreatment with frusemide not only fails to protect against the ARF but increases its severity. Isotonic saline adminstration and replacement of urinary losses almost prevent glycerol-induced ARF but when both isotonic saline frusemide are administered together their effect is only a slight increase in the excretion rate of urea and creatinine during the first days of the experiment. The importance of the changes in the ECV or a possible direct action of frusemide on the renin-angiotensin axis are discussed. There is a good correlation between plasma creatinine levels and interstitial oedema. The importance of the oedema in the maintenance of ARF is discussed.
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PMID:Negative effect of frusemide pretreatment in glycerol induced acute renal failure. 87 19

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

Blockade of prostaglandin synthesis with indomethacin (1) did not induce significant changes in blood pressure or in renal circulation in renovascular hypertensive rabbits with normal renal blood flow; (2) induced renal insufficiency and aggravated hypertension in hypertensive rabbits whose renal blood flow was below normal levels; (3) did not alter the reversal of renovascular hypertension produced by the release of the renal arterial constriction; and (4) induced a decrease in plasma renin activity by decreasing renin release. These findings indicate that the vasodilator and natriuretic actions of prostaglandins may play an important role in protecting the kidney against ischemia; the facilitating role of renal prostaglandins on renin release raises the possibility that a primary hypersecretion of renal prostaglandins is responsible for Bartter's syndrome, whereas a primary deficiency may be responsible for "low-renin hypertension."
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PMID:Hypertension and the interrelated renal circulatory effects of prostaglandins and the renin-angiotensin system. 87 71

Among eight patients with unilateral hydronephrosis and hypertension, peripheral plasma renin activity was normal in seven and borderline high in one. Four patients had hydronephrotic/contralateral kidney renin ratios of greater than 1.5, suggesting excessive renin release from the diseased kidney, and ratios between contralateral kidney and peripheral blood of less than 1.2, indicating suppressed renin production in the contralateral kidney. Nephrectomy normalized blood pressure in each of these patients. Two patients had hydronephrotic/contralateral kidney renin ratios of less than or equal to 1.3 or contralateral kidney/periphery ratios of greater than 1.2, suggesting ischemia of the contralateral kidney; pyeloplasty or nephrectomy, or both, failed to improve the hypertension. Postoperative changes in blood pressure correlated with changes in peripheral renin (r = 0.90; P less than 0.01). These data suggest that hypertension associated with unilateral hydronephrosis is partly renin-dependent; and renal vein renin values are helpful in selecting patients for surgery.
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PMID:Curable hypertension with unilateral hydronephrosis. Studies on the role of circulating renin. 90 42

An acute circulatory renal failure (ARF) was induced in 18 rabbits by temporary ischemia of the remaining kidney 8 days after unilateral nephrectomy and subcuteaneous autotransplantation of renomedullary tissue.--Mortality in the postischemic course was 50% in treated animals but 100% in the control group (n = 18) without autotransplantation. In the postischemic period plasma urea concentration was significantly lower (p smaller than 0.005) in the surviving transplanted animals and excretion of sodium and water significantly higher (p smaller than 0.005) as compared with the control group. Plasma renin values which were significantly lower than thos of the control(p smaller than 0.005) had decreased significantly even as compared with the initial values. These results indicate that hormonal substances are produced in interstitial cells of renomedullary autotransplants exerting a distinct protective effect against experimental acute renal failure. Decreased plasma renin activity may point to an inhibition of circulating and/or intrarenal renin by lipids originating from the transplants. Changes in sodium and water excretion indicate effects of circulating prostaglandins
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PMID:Experimental oliguric acute renal failure: protective effects of renomedullary autotransplants. 109 74

Reaction constants of renin in juxtaglomerular apparatus and plasma renin activity after renal ischemia and hemorrhage. During and after total renal ischemia and acute hemorrhage, renin activity in plasma (PRA) and microdissected juxtaglomerular apparatus (JGA) of rabbits were investigated. In controls, the apparent Michaelis-Mentoen constant (MMC) of semipurified standard renin of rabbits was 1025 plus or minus 223 SD ng/ml. Plasma renin of normal rabbits showed similar values: 1062 plus or minus 138 SD ng/ml. Intrarenal JGA renin, however, showed a great scatter of MMC (920 to 4760 ng/ml) and a significantly higher mean value of 2572 plus or minus 1156 SD ng/ml (pis less than 0.001). After complete renal ischemia by clamping both renal arteries for a 90-min period, the following results wereobtained: 1) Sixty min after the beginning of ischemia, PRA decreased from 20.9 plus or minus 9.8 SD to 7.6 plus or minus 5.2 SD ng/ml-hr (P is less than 0.05) and increased to 103, 68 and 42 ng/ml-hr 10, 30 and 90 min after removal of the clamps, respectively (P is less than 0.05).
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PMID:Reaction constants of renin in juxtaglomerular apparatus and plasma renin activity after renal ischemia and hemorrhage. 113 98

Evaluation of the concentration of atrial natriuretic peptide, angiotensin P, renin activity in the blood of the coronary sinus and aorta in 18 patients with IHD and hypertrophy of the left ventricle during development of induced ischemia revealed that in left ventricular hypertrophy secretion of atrial natriuretic peptide by the myocardium is reduced. The level of this reduction depends on the kind of hypertrophy. Dilatation of the left ventricle cavity furthers exhaustion of the secretory function of the ischemic myocardium.
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PMID:[The interrelation of the secretory activity of the myocardium with its hypertrophic characteristics in patients with ischemic heart disease]. 129 16


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