Abstract
The effect of the substances released from platelets and aggregating platelets on isolated canine basilar arteries was investigated by an isometric tension-recording method. Adenosine diphosphate (ADP) and adenosine triphosphate (ATP) relaxed the vascular tissue endothelium-dependently. Endothelium removal enhanced the dose-response curves to serotonin, but did not to carbocyclic thromboxane A. The suspension of platelets contracted canine basilar arteries dose-dependently. The contraction induced by platelets was augmented by endothelium removal. The serotonergic antagonists, ketanserin and methysergide inhibited the dose-response curves to platelets. However, a cyclooxygenase inhibitor, indomethacin did not shift the dose-response curves to platelets. The addition of platelets augmented the tension produced by 3 × 10-6M prostaglandin F2a. This augmentation was not affected by apyrase.
These results suggest that serotonin may play a major role in the contraction produced by platelets and that following endothelium removal, abolition of the release of endothelium-derived relaxing factor is the most probable mecahnism of the enhanced contraction.
