Abstract

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.

Highlights

  • Serotonin is a monoamine neurotransmitter and vasoactive substance with well described vascular actions

  • Taking into consideration that serotonin actions on the isolated carotid artery from different species are still under investigation, the present experiments were undertaken in order: (1) to examine the effect of serotonin on the isolated rat common carotid artery; (2) to investigate possible participation of intact endothelium and cyclooxygenase products in serotonin-evoked action; (3) to establish if Ca++ channels are important for transduction mechanism related to serotonin effect, and

  • Serotonin is endogenous monoamine that is involved in regulation and control of many physiological functions, including vascular resistance of different blood vessels

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Summary

Introduction

Serotonin is a monoamine neurotransmitter and vasoactive substance with well described vascular actions. In the vascular system serotonin predominantly induces endotheliumindependent vasoconstrictions after binding to serotonin 5-HT1 and 5-HT2 receptors that are located on the smooth muscle cells This is mainly described in the blood vessels of splanchnic region, kidneys, lungs and brain [1,2,3,4]. It has been established that intimal thickening, which is usually associated with endothelial dysfunction and advancement of atherosclerosis, may increase reactivity of this blood vessel to serotonin [13] This has a significant clinical importance considering that positive correlation between thickenings of intimal or muscular layer of carotid artery and subsequent cerebrovascular events has been established [14]. (3) to establish if Ca++ channels are important for transduction mechanism related to serotonin effect, and (4) to determine if serotonin 5-HT2 receptors are involved in serotonin-produced response of the investigated blood vessel

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