INVOLVEMENT OF RENIN-ANGIOTENSIN SYSTEM IN THE REDUCED PRESSURE NATRIURESIS RESPONSE OF HYPERTHYROID RATS

Previous studies have indicated that the pressure diuresis and natriur esis (PDN) response is greatly impaired in thyroxine-treated hypertens ive rats. In the present study, we have examined the role of the renin angiotensin system (RAS) as a mediator of these alterations by charac terizing the relationships between renal perfusion pressure and urine flow and sodium excretion in hyperthyroid rats acutely treated with a converting-enzyme inhibitor (captopril, 2 mg/kg) or an AT(1) angiotens in II receptor blocker (losartan, 10 mg/kg). In the control animals, c aptopril did not change mean arterial pressure (MAP) or renal blood fl ow (RBF) but significantly decreased MAP and increased RBF and glomeru lar filtration rate in the hyperthyroid rats. Captopril did not change the PDN response of the control animals but improved significantly th at of the hyperthyroid rats, although it was not completely normalized . Losartan also significantly improved renal hemodynamics and excretio n in hyperthyroid rats. These results indicate that an increased intra renal activity of the RAS is partly responsible for the blunted renal PDN mechanism of the hyperthyroid rats.