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

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

A simple method is presented for demarcation between different arterial areas, which allows the performance of nephrotomies with minimal bleeding and subsequent renal ischemia. The thermal gradient that exists between the segment with occluded blood supply and the adjacent ones retaining their blood supply is defined by a liquid cholesterol crystal sheet.
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PMID:Experimental and preliminary clinical experience with thermography for avascular nephrotomy. 71 89

Acute renal failure may be caused by multiple conditions including those which are due to some direct hemodynamic or nephrotoxic insult. In considering the pathophysiology of these entities, it seems appropriate to differentiate between the initiating and the maintenance phase of the disorder. In the former, renal ischemia and/or a direct effect of a given nephrotoxic agent seems to be the basis for the underlying renal damage. In the maintenance phase, renal functional impairment is maintained by a number of factors which include persistent renal vasoconstriction, tubular obstruction, a leakage of filtrate across damaged tubular epithelium, and a reduction in glomerular capillary permeability. The therapy and possible preventive aspects of these entities are discussed.
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PMID:Acute renal failure: clinical aspects and pathophysiology. 72 79

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

In the current study a) cardiovascular reactivity (CR) to norepinephrine (NE) and b) the effect of a ganglionic blocker (pentolinium, P) during the early (2nd week) and a later period (10th week) of hypertension elicited by unilateral renal ischemia and contralateral nephrectomy in the rat have been described. Neither the threshold doses nor the dose-pressor response curves have shown a greater reactivity of the cardiovascular system to NE in this type of hypertension. An increase in the activity of the nervous system apparently contributes to hypertension in the early period but would disappear when the one-kidney renovascular hypertension is chronically established; in both phases some other still undefined factor/s are present for fuller development of high arterial pressure.
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PMID:Cardiovascular reactivity and neurogenic tone in hypertension derived from renal artery stenosis and contralateral nephrectomy in the rat. 75 6

Renal phospholipid metabolism was studied after ischemia was induced by occlusion of the left renal artery in the rat. There was no change in the rate of cellular [14C]choline uptake after 25 or 60 minutes of ischemia. However, [14C]choline incorporation into phospholipid was two to three times greater in slices from the ischemic kidney than in slices from the contralateral control kidney. The increase occurred after 25 minutes of ischemia plus 15 minutes of reflow, and after 60 minutes of ischemia with or without reflow. When [14C]choline was injected into rats after a 60-minute period of renal ischemia, the rate of incorporation into phospholipid in the ischemic kidney was almost twice that of the control kidney. These results were similar to those of the in vitro experiments. Since virtually all of the cellular phospholipids of the kidney are present in cellular membranes, renal ischemia affects membrane metabolism. The mean distribution ratio of alpha-aminoisobutyric acid in slices of kidneys ischemic for 60 minutes was similar to that of control slices: 4.11 +/- 0.2 (SEM) vs. 4.30 +/- 0.30. The normal uptake of alpha-aminoisobutyric acid indicates that the increased incorporation of choline is associated with functional integrity of the membrane.
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PMID:Choline uptake into renal phospholipids following renal ischemia in rats. 75 33

Ten rabbits with transparent ear chambers were grafted with small pieces of kidney. The resulting vessel anastomosis and restoration of renal blood flow allowed continuous microscopic observations of functioning renal tissue in vivo. When the grafts were well established, acute renal failure was induced in the rabbit by glycerol injection. All cases showed similar changes. Within minutes the brisk blood flow within the renal grafts became progressively more sluggish until complete stasis was established. The initial change was a blanching of intertubular and glomerular capillaries with progressive dilation and stasis of renal veins. Only after almost complete cessation of blood flow in most graft vessels, generally after a further 10 minutes, was any change in arteries or arterioles observed. The afferent arterioles and then larger arteries showed constriction followed by complete stasis. The ear chamber vessels (nonrenal) continued to flow normally. Blood flow was slowly re-established in the grafts and by the next day was normal in the surviving rabbits. These studies provided visual in vivo evidence that the mechanism of glycerol-induced acute renal failure is mediated by a reversible renal ischemia and that the factors responsible act particularly on renal vasculature. However, the mechanism whereby blood flow ceases is obscure and it cannot be attributed to arterial or arteriolar constriction.
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PMID:The mechanism of glycerol-induced acute renal failure. 77 14

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


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