741 CARDIAC AND RENAL PROTECTIVE EFFECTS OF HEPATOCYTE GROWTH FACTOR (HGF), INDUCED BY IRBESARTAN IN MOUSE MODEL OF SALT-SENSITIVE HYPERTENSION

s e215 of each period, we measured 1. ABP, 2. CBP, 3. Free water clearance (CH2O), fractional excretion of sodium (FENa) and potassium (FEK), urinary excretions of aquaporin 2(u-AQP2/min), and the γ fraction of the epithelial sodium channel per minute (u-ENaCγ), and 4. Plasma concentrations of renin (PRC), angiotensin II (p-Ang II), and aldosterone (p-Aldo). Examinations were done both at baseline conditions and after furosemide iv. Results During baseline conditions, there were no differences in ABP, CBP, renal tubular function, or plasma concentrations of vasoactive hormones. After furosemide, an increase in CBP, CH2O, FENa, FEK, u-AQP2/ min, u-ENaCγ/ min, PRC, p-Ang II, p-Aldo was observed. Furosemide induced a more pronounced effect on CBP, p-Ang II, p-Aldo after amiloride and spironolactone than placebo. Conclusion The more pronounced increases in central systolic blood pressure after amiloride and spironolactone treatment than placebo can be due to a greater increase in the activity of the renin-angiotensin-aldosterone system. The increases in water and sodium absorption via AQP2 and ENaC after furosemide most likely are compensatory phenomena to antagonize water and sodium depletion.