Diuretic-induced changes in renal blood flow and prostaglandin E excretion in the dog

Publisher Website
Google Scholar
Abstract
Commonly used diuretic agents have a direct inhibitory effect on electrolyte transport in 1 or more nephron segments, and apparently the hemodynamic effect of a given agent may be a determinant of the magnitude of the change in Na excretion (UNaV). Studies have shown that indomethacin blunts the vasodilating and natriuretic action of furosemide suggesting that renal prostaglandin E (PGE) production may mediate the hemodynamic change caused by furosemide. To further evaluate this possibility and to determine whether there is a correlation between renal PGE production and the hemodynamic response to diuretic administration, studies were performed in the dog in which 2 vasodilating diuretics and 2 agents which tend to decrease renal blood flow were evaluated. Furosemide and ethacrynic acid caused significant increases in renal blood flow, UNaV, and urinary excretion of PGE (UPGEV). Chlorothiazide and benzolamide also increased UNaV. In contrast to furosemide and ethacrynic acid, renal blood flow was either unchanged or decreased after both chlorothiazide and benzolamide. Chlorothiazide or benzolamide did not significantly alter UPGEV. UPGEV is increased after furosemide and ethacrynic acid, which is consistent with the view that the hemodynamic effect of these agents is mediated by enhanced renal PGE production.