Next Article in Journal
Absorption, Distribution and Excretion of 14C-Probimane in Mice Bearing Lewis Lung Carcinoma
Previous Article in Journal
Production, Quality Control and Pharmacokinetic Studies of 166Ho-EDTMP for Therapeutic Applications
Article Menu

Article Versions

Export Article

Open AccessArticle
Sci. Pharm. 2010, 78(3), 435-444; doi:10.3797/scipharm.1004-04

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

Department of Pharmacology, Clinical Pharmacology and Toxicology; Medical Faculty; University of Belgrade; PO Box 38; 11129 Belgrade; Serbia
*
Author to whom correspondence should be addressed.
Received: 5 April 2010 / Accepted: 15 June 2010 / Published: 15 June 2010
Download PDF [266 KB, uploaded 29 September 2016]

Simple Summary

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.
Keywords: Serotonin; Common Carotid Artery; Endothelium; Thromboxane A2 Serotonin; Common Carotid Artery; Endothelium; Thromboxane A2
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

Scifeed alert for new publications

Never miss any articles matching your research from any publisher
  • Get alerts for new papers matching your research
  • Find out the new papers from selected authors
  • Updated daily for 49'000+ journals and 6000+ publishers
  • Define your Scifeed now

SciFeed Share & Cite This Article

MDPI and ACS Style

RADENKOVIĆ, M.; STOJANOVIĆ, M.; TOPALOVIĆ, M. Contribution of Thromboxane A2 in Rat Common Carotid Artery Response to Serotonin. Sci. Pharm. 2010, 78, 435-444.

Show more citation formats Show less citations formats

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Sci. Pharm. EISSN 2218-0532 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top