Renal actions of prostacyclin

A NEW and important member of the arachidonate–thromboxane–prostaglandin system, prostacyclin (PGI 2 ), has recently been isolated 1–3 . This bicyclic prostaglandin has been shown to be synthesised from the prostaglandin endoperoxides PGG 2 and PGH 2 , by arteries, veins, heart and other tissues in several species, including man 1–7 . PGI 2 is a powerful inhibitor of platelet aggregation and relaxes arterial strips 1,2,4,5 . It is 30 times more potent than PGE 1 as an inhibitor of platelet aggregation, and in the intact dog promotes a dramatic reduction in systemic blood pressure 1,2,8,9 . It has also been suggested that PGI 2 is a potent coronary vasodilator and anti-atherogenic compound 10–12 , and that it plays an essential part in the homeostasis of the cardiovascular system 1,2,4,5,11,12 . The kidneys receive a large portion of the cardiac output and have an extensive vascular tree, and so PGI 2 may be extremely significant in regulating kidney function. Human and rabbit renal cortical microsomes have been found to convert PGG 2 to PGI 2 (ref. 13), but nothing is known of the renal effects of PGI 2 . Therefore, this study was designed to evaluate the effects and significance of an intrarenal infusion of PGI 2 on renal haemodynamics, urinary function and renal vein plasma renin activity, and to compare these effects with those produced by PGE 2 and PGD 2 , two prostaglandins known to be synthesised by the kidney and to affect renal function.