A possible molecular basis of natriuresis during ischemic-reperfusion injury in the kidney.

Journal of the American Society of Nephrology : JASN
Z WangM Soleimani

Abstract

Ischemic renal injury is associated with increased fractional excretion of sodium, suggesting a Na+ reabsorption deficiency in renal tubules. To determine whether alterations in expression of the major Na+ transporter genes might contribute to the natriuresis that follows ischemic acute renal failure, the expression of these genes was analyzed in renal cortex and medulla after ischemic-reperfusion injury. Rats were subjected to 30 min of renal pedicle clamping and then sacrificed at 12, 24, or 48 h after reperfusion. Serum creatinine increased significantly at 12 and 24 h, indicative of acute renal failure, but decreased substantially by 48 h. mRNA levels for the NHE-3 Na/H exchanger of the proximal tubule, the apical Na-K-2Cl cotransporter of the thick ascending limb of Henle, the Na-Cl cotransporter of the distal convoluted tubule, the epithelial Na+ channel of the collecting duct, and the basolateral Na(+)-K(+)-ATPase were measured by Northern hybridization. NHE-3 mRNA decreased by approximately 75% at 12 h and remained suppressed at 24 and 48 h after reperfusion. Na-K-2Cl cotransporter mRNA decreased by approximately 88% at 12 h and remained suppressed at 24 and 48 h. Na-Cl cotransporter mRNA remained unchanged at 12 h, dec...Continue Reading

Citations

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