Responses of isolated feline and human cerebral arteries to prostacyclin and some of its metabolites.

The effects of prostacyclin (PGI2) were studied in isolated cat basilar and middle cerebral arteries and in human pial arteries. In feline vessels with low resting tension, PGI2 had a contractile effect that reached a maximum of 132% (basilar artery) and 23% (middle cerebral artery) of the potassium-induced (127 mM) contraction. In potassium-contracted feline vessels, PGI2 caused a further contraction. When these vessels were contracted by PGF2 alpha, PGI2 induced relaxation, which was most marked in the middle cerebral artery. PGI2 consistently relaxed the middle cerebral artery contracted by the prostaglandin endoperoxide analogue U-44069, whereas the basilar artery was almost unaffected. In human pial arteries with low resting tension, PGI2 had no effects in concentrations below 10(-6) M, whereas higher concentrations induced contractions. In potassium-contracted (35 or 127 mM) preparations, PGI2 in concentrations below 10(-6) M produced relaxation; in higher concentrations further contraction was induced. Human pial arteries contracted by PGF2 alpha, U-44069, noradrenaline, or 5-hydroxytryptamine consistently relaxed in response to PGI2 (less than 10(-6) M). The PGI2 metabolite 6-keto-PGE1 had effects similar to those of PGI2, but proved to be less potent on human pial vessels. 6-Keto-PGF1 alpha was ineffective, whereas 6,15-diketo-PGF1 alpha had minor relaxant effects. The results suggest that consideration must be given to regional as well as species differences concerning the cerebrovascular effects of PGI2.