Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0920646 (renal ischemia)
 2,515 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recently, it has been reported that atrial natriuretic peptide (ANP) reverses or prevents acute renal failure induced by norepinephrine in rats. Therefore, we tested the hypothesis that vasoconstrictor doses of arginine vasopressin (VP) can induce renal ischemia and that consequent renal dysfunction is reversed by ANP infusion or bolus injections in rats. Intrarenally infused VP produced a significant decrease of glomerular filtration rate (GFR) and an increase of urinary volume and sodium excretion rate. Systemic blood pressure increased significantly during VP administration. In a second experimental period, ANP was also given intrarenally, control rats received isotonic saline solution. ANP infusion revealed a highly significant increment of GFR, urinary volume and sodium excretion. Blood pressure fell down below values of the preperiod. After cessation of ANP infusion, renal function was reduced again. These results indicate that VP induces a nonoliguric acute renal failure which is reversed by ANP infusion but only at the time of its administration.
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PMID:Atrial natriuretic peptide reverses experimental acute renal failure induced by arginine vasopressin. 213 64

The present work was performed on uninephrectomized rabbits recovering from ischemic acute renal failure (ARF) in an attempt to elucidate whether or not intraglomerular events are a determinant factor in the development of resistance to ARF. 14 days after a 2-hour clamping of the renal artery (the recovery phase), the animals did not show resistance to an additional ischemia. On the other hand, glomeruli derived from normal kidneys displayed a contractile response to angiotensin II, arginine vasopressin or norepinephrine in Eagle's minimum essential medium, whereas glomeruli from rabbits recovering from ischemic ARF were refractory to the vasoconstrictor agents. The findings suggest that glomerular refractoriness to contractile stimuli does not provide resistance to an additional renal ischemia in the ischemic model of ARF.
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PMID:Glomerular refractoriness to contractile stimuli in rabbits recovering from ischemic acute renal failure. 336 77

Endothelin is an important modulator of renal function via its binding to abundant receptors in renal tissue and by the ability of renal endothelial and epithelial cells to synthesize and release endothelin. In the kidney, endothelin may function as a paracrine-autocrine factor in the regulation of renal blood flow, glomerular hemodynamics, and sodium and water homeostasis. Recent evidence suggests that circulating endothelin may play an important role in renal regulation in cardiorenal states of endothelin activation. Endothelin is a potent renal vasconstrictor that has dual actions on glomerular filtration rate due to its ability to preferentially constrict efferent arterioles preserving glomerular filtration. Furthermore, endothelin modulates sodium excretion and water balance at the level of the proximal tubule and medullary collecting ducts, respectively, by mechanisms that are still unclear. In addition, endothelin stimulates the renin-angiotensin-aldosterone system and atrial natriuretic peptide release and inhibits arginine vasopressin-mediated water reabsorption in the inner medullary collecting duct. Recent studies using specific receptor antagonists have demonstrated a pathophysiologic role for endothelin during renal ischemia, cyclosporine-induced toxicity, and chronic renal failure. This review highlights recent research that supports an important role for endothelin as a locally produced vasoactive and natriuretic peptide in the regulation of renal hemodynamic and excretory functions.
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PMID:Physiologic and pathophysiologic roles of endothelin in the kidney. 785 Apr 14