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Abstract The effects of the antimicrotubular drugs colchicine and vinblastine on the blood platelet release reaction were studied by measuring release of 14 C‐5‐hydroxytryptamine ( 14 C‐5‐HT, release I) and β‐glucuronidase (release II) from gel‐filtered human platelets. β‐glucuronidase release induced by thrombin was significantly inhibited by colchicine (0.01‐1 mM) or vinblastine (0.05–0.1 mM). Release of 14 C‐5‐HT, however, was unaffected at low concentrations of colchicine and only slightly inhibited at higher concentrations. Inhibition of β‐glucuronidase release depended on colchicine or vinblastine concentrations and decreased with longer time intervals (1′, 5′, 20′) after thrombin stimulation. Levels of the cytoplasmic enzyme, lactic acid dehydrogenase, in supernatants of colchicine treated platelets were not significantly different from controls. Colchicine also inhibited β‐glucuronidse release, but not 14 C‐5‐HT release, induced by trypsin and sodium arachidonate. Binding of 14 C‐colchicine by platelets was measured and it was found that platelet aggregation and release of 5‐HT induced by adenosine diphosphate, epinephrine and collagen proceeded without any alteration in colchicine binding. However, significant increases in the rate and degree of colchicine binding were observed when platelets were stimulated by thrombin, trypsin and arachidonic acid which induced aggregation, release of both 5‐HT and β‐glucuronidase. The results suggest that an alteration in platelet microtubules is correlated with the physiologic response resulting in release II and that the cellular mechanisms effecting release I and II by platelets differ qualitatively in that the microtubules may facilitate release II.
Kenney et al. (Sat,) studied this question.