Increased Renal Potassium Secretion Associated with Increased Vasopressin Prevents Hyperkalemia in a Rat Model of Hemorrhagic Shock

Abstract

Trauma is the leading cause of death in young adults worldwide, and up to 50% of these deaths involve hemorrhage. Hyperkalemia is associated with non‐survival of severe hemorrhage. During shock, urine flow is dramatically decreased, and thus, in order to maintain electrolyte balance, renal handling of solute secretion must be altered. In this study, we tested the hypothesis that the kidneys respond to hemorrhage by increasing potassium (K) secretion to prevent hyperkalemia. We compared renal handling of K and sodium (Na) in conscious, chronically‐catheterized rats (n=15) before, during, and after hemorrhage (2 ml shed blood/100 g body weight, 25% hematocrit decrease). One hour after hemorrhage, rats were resuscitated with normal saline. With shock, urine flow decreased from 14 ± 2 to 4 ± 1 ul/min/100g BW, and osmotic clearance also concomitantly decreased (34 ± 3 to 15 ± 2 ul/min/100g, p<0.05). There was a slight increase in plasma K (3.94 ± 0.06 to 4.34 ± 0.07 mEq/L, p<0.05) during hemorrhage. Endogenous plasma vasopressin (VP) levels increased (5.3 ± 1.2 to 26.8 ± 8.4 pg/ml, p<0.05), followed by an increase in renal trans‐tubular K gradient (11 ± 1 to 14 ± 1, p<0.05). Urine K levels increased (111 ± 13 to 191 ± 10 mEq/L, p<0.05) whereas urine Na levels did not. Results suggest that a relative increase in renal tubular K secretion mediated by VP plays an important role in the regulation of K homeostasis during hemorrhage. This increase in K secretion may protect against hyperkalemia in hemorrhagic shock.