Contribution of Thromboxane A₂ in Rat Common Carotid Artery Response to Serotonin

Serotonin is a vasoactive substance that in different blood vessels mostly induces vasoconstriction. Considering the important role of common carotid artery in brain blood supply, the aims of this study were to investigate the effect of serotonin on isolated rat common carotid artery and also to examine participation of intact endothelium, cyclooxygenase products, Ca⁺⁺ channels and 5-HT₂ receptors in serotonin-evoked action. Endothelium was mechanically removed from some vascular rings. Circular artery segments were placed in organ baths containing Krebs–Ringer bicarbonate solution. Cumulative concentration-contraction curves for serotonin were obtained in rings previously equilibrated at basal tone. Serotonin produced concentration-dependent contraction, which was unaltered by endothelial denudation. Serotonin-induced effect was notably and comparably reduced by indomethacin (cyclooxygenase inhibitor) or OKY–046 (thromboxane A₂-synthase inhibitor) on intact or denuded rings. Nifedipine (Ca⁺⁺ channel blocker) or ketanserin (5-HT₂ receptor antagonist) strongly reduced serotonin-evoked effect. Our results suggest that serotonin produced concentration-dependent and endothelium-independent contraction of carotid artery, which was initiated by activation of 5-HT₂ receptors located on smooth muscle cells and mediated via L-type Ca⁺⁺ channels. Thromboxane A₂ from smooth muscle cells notably contributed to the overall contraction of carotid artery induced by serotonin.