Effect of spironolactone and benazepril on furosemide-induced diuresis and renin-angiotensin-aldosterone system activation in normal dogs.

The neurohormonal profile during FCRI supports RAAS mediation of diuretic braking in this model. Background treatment with benazepril with or without spironolactone did not mitigate braking, but was well tolerated. Delayed changes in sCr and serum sodium concentration and incomplete recovery of hydration indicators caused by furosemide hold implications for clinical patients.