Abstract 377: Expression of Soluble and Full-length (pro)renin Receptor by Dehydration
Recently, (pro)renin receptor ((P)RR), a specific receptor for renin and prorenin, was newly identified as a member of the renin angiotensin system (RAS). (P)RR binding to the prorenin, causes the generation of angiotensin II via the increased enzymatic activity. (P)RR exists in two forms, one is full-length form (f(P)RR), and the other is soluble form (s(P)RR). RAS as well as vasopressin system contributes to the regulation of body fluid balance in a state of dehydration, but roles of (P)RR are unidentified. The purpose of this study was to examine the effects of dehydration on (P)RR expression in the plasma, the urine and kidney. Twelve week-old, male Wister Kyoto rats (n=10) were randomly divided into two groups, and the dehydration was induced by water restriction for 72 h in metabolic cage. Food intake and urinary output were measured. After 72h, rats were killed, and the protein expression of (P)RR in the plasma, the urine and kidney was investigated by using Western blotting. Compared with control rats, dehydration significantly increased osmotic pressure in the plasma and urine (286.8±2.9 vs 305.6±16.8 mOsm/L, p<0.05, 409.0±450.6 vs 1566.0±381.5 mOsm/L, p<0.01, respectively). Similarly, dehydration significantly increased in plasma renin activity and angiotensin II(8.5±3.8 vs 13.5±2.8 ng/ml/h, 409.6±175.6 vs 3595.6±1086.9 pg/ml, p<0.01, respectively). Dehydration decreased the s(P)RR expression in the plasma, but increased in the urine (0.3-fold, 1.5-fold respectively) by direct Western blotting. Dehydration increased the f(P)RR expression levels in the renal homogenates, microsome fraction, and cytosol fraction (2.3-fold, 3.0-fold, 22.9-fold respectively). Dehydration tended to decrease s(P)RR in renal cytosol, but it had no significant difference. These results indicated that dehydration increased the f(P)RR expression in the kidney with the downregulation of s(P)RR levels in the plasma, suggesting a specific stimulation of renal RAS by (P)RR.
- © 2012 by American Heart Association, Inc.