Thrombin-induced platelet release reaction examined with secretion of calcium and
N-acetylglucosaminidase was significantly enhanced in the platelets from reserpine-treated
rabbits as compared with the control. On the other hand, 32P-incorporation into phosphatidic acid was suppressed in the reserpinized platelets
in activated state. Thrombin induced phosphatidylinositol (PI)- breakdown, which was
examined by decreases in radioactivity and content of PI, and an increase in diacylglycerol,
was not enhanced in the reserpinized platelets as compared with the control. The phosphorylation
of the specific protein coupled to thrombin- induced platelet PI-breakdown was not
stimulated in the reserpinized platelets as compared with the control. In contrast
to PI, PC-degradation by thrombin was significantly stimulated in the reserpinized
platelets. Possible existence of pathway(s) other than that associated with an enhancement
of Pl-tumover is conceivable as a mechanism involved in platelet release reaction.
Keywords
Platelet release reaction - Reserpine - Phosphatidylinositol response - Thrombin
