Thirst and sodium appetite in rats with experimental nephrotic syndrome

•Injections of Adriamycin were used to create a model of nephrosis in rats.•Adriamycin treatment attenuated water drinking to renin-dependent challenges.•Adriamycin treatment reduced sodium intake after acute hypovolemic challenge.•Adriamycin treatment attenuated release of renin and aldosterone to isoproterenol.•Water drinking to osmotic challenge and angiotensin II were not affected.

Nephrotic syndrome is a renal disease accompanied by abnormal body fluid balance. The present experiments investigated the role of behavioral mechanisms in contributing to disordered fluid homeostasis in rats with experimentally-induced nephrotic syndrome. The studies examined water and sodium ingestion under ad libitum conditions and in response to dehydration-related challenges in rats made nephrotic by treatment with the antibiotic, adriamycin. Rats with nephrotic syndrome had greater ad libitum water intakes beginning 3 weeks after treatment, but daily sodium (0.3 M NaCl) intakes were not affected. Nephrotic rats showed attenuated water and sodium intakes after combined treatment with furosemide (10 mg/kg) and captopril (2 mg/kg), reduced water intakes after 20 h of water deprivation, and diminished water intakes, plasma renin activity and aldosterone secretion after subcutaneous isoproterenol (30 μg/kg). However, the adriamycin-treated animals had normal water intakes in response to subcutaneous hypertonic saline (4% at 0.75 ml/100 g) and central injections of angiotensin II (10, 20, and 50 ng). The results suggest that water and sodium ingestion in response to hypovolemic/hypotensive stimuli are disturbed in nephrotic rats, and provide evidence that the disordered behaviors reflect disturbances of the peripheral renin-angiotensin-aldosterone system.