Release of a Prostaglandin E-Like Substance from Canine Kidney by Bradykinin

Abstract

Renal vasodilation produced by two dissimilar vasodepressor polypeptides, bradykinin and eledoisin, was correlated with changes in renal venous concentrations of substances having the properties of prostaglandins of the E and F series in anesthetized dogs. Samples of renal venous blood were extracted for acidic lipids, and the prostaglandin E and prostaglandin F zones of the chromatographed extracts were eluted and assayed in vitro for prostaglandins of the E and F series by a parallel bioassay system (sensitivity 0.015 ng/ml blood). During the first 2 minutes of infusion, bradykinin increased the concentration of a prostaglandin E-like substance in renal venous blood from a mean control level of 0.16 ng/ml to 1.05 ng/ml ( P <0.01); this increase occurred simultaneously with the greatest increase in renal blood flow to 432 ml/min from a control value of 282 ml/min. After 12 minutes of bradykinin infusion, the concentration of the prostaglandin E-like substance had decreased to 0.30 ng/ml, and renal blood flow had fallen to 398 ml/min. In contrast, eledoisin infused in equidilator doses did not increase the concentration of the prostaglandin E-like substance. The concentration of prostaglandin F-like substances was not affected by either polypeptide. A transient increase in urine flow occurred during the first 2 minutes of bradykinin infusion only. These results suggest that a prostaglandin E-like substance participates in the renal vasodilator and the diuretic responses to bradykinin.

Captopril inhibits endothelin-1 secretion from endothelial cells through bradykinin.

“…ACE inhibition decreases not only formation of angiotensin II 8 but also degradation of kinins. 18 In cultured human and bovine endothelial cells, ACE inhibitors elevate intraceUnlar calcium concentrations and stimulate the production of NO and prostaglandin I 2 via Bj receptors. 14 In the present study, the enhancement of NO production by captopril was inhibited by coincubation with the Bj receptor antagonist.…”

Prostaglandins and the mechanism of analgesia produced by aspirin‐like drugs

“…We have not attempted to characterize further the prostaglandin(s) released, but in other dog and cat spleen perfusions the release was predominantly of prostaglandin E2 (Davies, Horton & Withrington, 1968;Gilmore et al, 1968;Ferreira, Moncada & Vane, 1973). Bradykinin also causes release of prostaglandin E2 from dog kidney (McGiff, Terragno, Malik & Lonigro, 1972). The relative effects of the prostaglandin-like material on the assay tissues we used, together with the fact that a specific inhibitor of prostaglandin biosynthesis prevented its release, suggest that here, also, it was mainly a prostaglandin of the E series.…”

Contribution of NO and cytochrome P450 to the vasodilator effect of bradykinin in the rat kidney

“…Thus, in rat skeletal muscle the vasodilator effect of bradykinin appears to be mediated primarily by prostaglandins (Messina et al 1975) while in the canine kidney, the vasodilator effect of bradykinin is associated with the release of prostaglandins (McGiff et al, 1972). Further, in the cat cerebral vasculature, bradykinin stimulates the release of oxygen-derived free radicals (Kontos et al, 1984), generated as a result of cyclooxygenase metabolism of arachidonic acid which is released consequent to stimulation of phospholipases.…”