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excretion and plasmin activity were not substantially increased. Accordingly, CM did not prevent hypertension in SHR (SBP (mmHg): SHR 162 vs. SHRþCM 158). In Experiment 2, HS diet induced severe hypertension, marked proteinuria and plasmin activation in urine in SHR/ND mcr-cp. These changes were significantly suppressed by the treatment with CM (SBP (mmHg): HS 230 vs. HSþCM 178; urinary protein (mg/ day): HS 331 vs. HSþCM 86) with the concomitant increase of urinary sodium/potassium ratio, indicating that CM inhibited the ENaC activity. Because CM markedly attenuated proteinuria, we further examined the effect of CM on podocyte injuries. Although CM did not affect body weight, glucose metabolism and adipokine expression in the adipose tissue, it suppressed glomerulosclerosis, the downregulation of nephrin and synaptopodin, and apoptosis of podocytes induced by HS diet. CM also suppressed apoptotic molecules activation by high glucose and aldosterone in cultured murine podocytes.

SP073IN OBESE ZSF1 RATS, FEMALES SHOW INCREASED SALT-SENSITIVITY COMPARED TO MALES