Renal actions of prostacyclin

Abstract

A NEW and important member of the arachidonate–thromboxane–prostaglandin system, prostacyclin (PGI2), has recently been isolated1–3. This bicyclic prostaglandin has been shown to be synthesised from the prostaglandin endoperoxides PGG2 and PGH2, by arteries, veins, heart and other tissues in several species, including man1–7. PGI2 is a powerful inhibitor of platelet aggregation and relaxes arterial strips1,2,4,5. It is 30 times more potent than PGE1 as an inhibitor of platelet aggregation, and in the intact dog promotes a dramatic reduction in systemic blood pressure1,2,8,9. It has also been suggested that PGI2 is a potent coronary vasodilator and anti-atherogenic compound10–12, and that it plays an essential part in the homeostasis of the cardiovascular system1,2,4,5,11,12. The kidneys receive a large portion of the cardiac output and have an extensive vascular tree, and so PGI2 may be extremely significant in regulating kidney function. Human and rabbit renal cortical microsomes have been found to convert PGG2 to PGI2 (ref. 13), but nothing is known of the renal effects of PGI2. Therefore, this study was designed to evaluate the effects and significance of an intrarenal infusion of PGI2 on renal haemodynamics, urinary function and renal vein plasma renin activity, and to compare these effects with those produced by PGE2 and PGD2, two prostaglandins known to be synthesised by the kidney and to affect renal function.