LACK OF RENAL DOPAMINE PRODUCTION DURING ACUTE VOLUME EXPANSION IN DAHL SALT-SENSITIVE RATS

Endogenous kidney dopamine (DA) is reported to contribute to the natri uretic response to acute volume expansion (VE). Several studies sugges t that a defect in renal DA-ergic system may play a role in genetic hy pertension in humans and rats. The present study was performed to dete rmine the role of renal DA and tubular DA-1 receptors in the natriuret ic response to VE in age-mached inbred Dahl salt sensitive (SS/Jr) and salt resistant (SR/Jr) rats of 9-11 weeks of age. In pentobarbital an esthetized rats, VE was carried out by intravenous infusion of isotoni c sodium chloride (5% body weight) over a period of 60 min. This maneu ver evoked marked increases in urine output and urinary sodium excreti on in both SR/Jr and SS/Jr species. However, the natriuretic and diure tic response to VE was significantly reduced in SS/Jr as compared to S R/Jr rats. It was also observed that the urinary excretion of DA was s ignificantly increased during VE only in SR/Jr, but not in SS/Jr rats. In separate group of animals, infusion of DA (1 mu g/kg/min) produced similar increases in urine output and urinary sodium excretion withou t causing any alterations in blood pressure or heart rate in either SS /Jr or SR/Jr rats. These results suggest that SS/Jr rats are not able to eliminate an acute increase in sodium load as efficiently as SR/Jr, which may be partly due to an impaired endogenous kidney DA productio n.