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The hemolysate (10(-5)-10(-2) times dilution; original hemoglobin concentration was 0.83 +/- 0.10 X 10(-3)M) evoked the contraction in a dose dependent manner, and this contraction was composed of low and high sensitive responses as estimated from the Eadie-Hofstee's plot. Indomethacin (10(-7)-10(-5)M) inhibited the latter component in the hemolysate-induced contraction. The membrane potential of smooth muscle cells was -50 mV and the cell was electrically quiescent. The hemolysate (greater than 10(-2) times dilution) depolarized the membrane and increased the ionic conductance of membrane. In rare occasions, the spike potential was triggered on the hemolysate-induced depolarization. The hemolysate (10(-5)-3 X 10(-3) times dilution) produced the contraction with no change in the membrane property. Carbocyclic thromboxane A2 ( cTXA2 ; 2.8 X 10(-10)M) produced the contraction without depolarization of the membrane, yet the TXA2 synthesis inhibitor, OKY-1581 (10(-5)M), had no effect on the hemolysate-induced contraction. PGE1, PGE2 and PGF2 alpha (2.8 X 10(-6)M) produced the contraction with no change in the membrane property. The contraction evoked by 2.8 X 10(-6)M PGF2 alpha corresponded well with that evoked by 3 X 10(-3) times dilution of the hemolysate. Removal of the endothelium by mechanical rubbing modified the hemolysate-induced contraction. Under the assumption that OKY-1581 is a selective inhibitor for TXA2 synthesis, the major part of the contraction (the indomethacin sensitive component) of the basilar artery is postulated to be due to synthesis of the primary PG rather than TXA2 by the hemolysate, yet the hemolysate itself, has to some extent a direct action in evoking the small contraction.

Hemolysate-induced contraction in smooth muscle cells of the guinea pig basilar artery.