Received June 5, 2007
Revised July 11, 2007
Accepted after revision August 23, 2007

¹ Indian Veterinary Research Institute

^* To whom correspondence should be addressed. E-mail: smishraivri{at}rediffmail.com.

	Abstract

Cerebral ischemia is considered to be an important cause of central nervous system dysfunction in heat stress. We hypothesized that heat stress would alter the reactivity of isolated carotid artery to vasoactive agents. Carotid arteries were isolated from broiler chicken, maintained either at 23-24°C with 55-65% humidity(control) or exposed to 40±1°C with 35% humidity for 4 h (heat stress). Contractions were elicited with vasoconstrictors like, 5-HT, phenylephrine, guanfacine and CaCl2 (K+-depolarized) in endothelium-denuded rings. Heat stress significantly increased the potency of 5-HT, but had no effect on the sensitivity of the vessel to phenylephrine and guanfacine. In contrast, it markedly decreased the potency and efficacy of CaCl2. Vasodilator responses to ACh (endothelium-intact) and sodium nitroprusside (endothelium-denuded), however, were unaffected. Although, cyclopiazonic acid (CPA; 10 µM) significantly decreased 5-HT responses in both the conditions, the agonist was still more potent in heat stress. Extracellular Ca2+ removal had no effect on contractions caused by 5-HT in controls, but it significantly decreased the agonist potency in heat stress. Interestingly, nifedipine (1 µM) markedly inhibited 5-HT contractions both in control and heat stress, implying its inhibitory effect on both Ca2+ influx and release. Thus, nifedipine had a markedly greater inhibitory effect on 5-HT contractions in heat stress compared to controls. The results suggest that heat stress increased the vasoconstrictor responses to 5-HT by a mechanism that involved extracellular Ca2+-influx through the nifedipine-sensitive L-type calcium channels.

Key Words: Heat stress, Serotonin, Vasoconstriction