Abstract
In anesthetized dogs, the diuretic furosemide has been shown to increase renal blood flow, an effect which can be blocked by the prostaglandin synthetase inhibitor, indomethacin (1, 2). Furosemide also caused an increase in PGE2 release into renal venous blood and this increase was inhibited by indomethacin (2). These data suggest a relationship between the hemodynamic effect of furosemide and the renal prostaglandins.
PGE2 is a vasodilator in the dog kidney; however, Malik and MgGiff (3) demonstrated that this prostaglandin increases renal vascular resistance in the rat. This apparent species difference between the rat and other mammals (4) offers a potential tool for elucidating the relationship between furosemide and PGE2 on renal hemodynamics. If the action of furosemide to dilate the renal vasculature in dogs is dependent on release of PGE2, and if PGE2 is a vasoconstrictor in rats, then furosemide would be expected to decrease renal blood flow in the rat. Alternatively, if the primary effect of furosemide is to produce hemodynamic changes which secondarily influence prostaglandin synthesis, furosemide might increase renal blood flow in rats as it does in dogs.
The purpose of this investigation was to determine the effect of furosemide on renal vascular resistance and to elucidate the interactions between this diuretic and PGE2 in isolated perfused rat kidneys. Since the renin-angiotensin system may also influence the renal vasculature, experiments were performed to evaluate interactions between this system and PGE2 and furosemide.
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