Effect of P2-purinoceptor antagonists on hemolysate-induced and adenosine 5'-triphosphate-induced contractions of dog basilar artery in vitro.

Abstract

To test the hypothesis that the vasoactive effects of hemolysate of dog erythrocytes on dog basilar artery in vitro are caused by adenosine 5'-triphosphate (ATP). Dog erythrocyte hemolysate was assayed for ATP by high-pressure liquid chromatography. Dog basilar arteries were cut into rings and studied under isometric tension to determine the effects of the P2-purinoceptor antagonists suramin, pyridoxal phosphate-6-azophenyl-2',4'-disulfonic acid, and reactive blue 2 on contractions induced by hemolysate, prostaglandin F2 alpha (PGF2 alpha), KCl, uridine 5'-triphosphate, and ATP. Dog erythrocyte hemolysate contained 34 mumol/L of ATP. Hemolysate produced concentration-dependent contractions of dog basilar artery. Suramin (100 mumol/L) significantly inhibited contractions to hemolysate, ATP, and uridine 5'-triphosphate but not to PGF2 alpha and KCl (P < 0.05). Pyridoxal phosphate-6-azophenyl-2',4'-disulfonic acid (100 mumol/L) caused a small but significant reduction of the contractions to hemolysate and did not affect contractions to PGF2 alpha and KCl. Reactive blue 2 (30 mumol/L) produced significant inhibition of contractions to hemolysate and PGF2 alpha but did not affect contractions to KCl. These findings suggest that ATP mediates a smooth muscle contractile response of hemolysate on dog basilar artery. Because erythrocyte cytosol is known to be important in the pathogenesis of vasospasm, these results suggest that ATP may contribute to the vasoconstriction that occurs in vasospasm.