J. Garciaestan et al., INVOLVEMENT OF RENIN-ANGIOTENSIN SYSTEM IN THE REDUCED PRESSURE NATRIURESIS RESPONSE OF HYPERTHYROID RATS, American journal of physiology: endocrinology and metabolism, 31(5), 1995, pp. 897-901
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.