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This Article Full Text Full Text (PDF) All Versions of this Article: 92/6/1077    most recent expphysiol.2007.038844v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Siddegowda, Y. K. B. Articles by Mishra, S. K. Search for Related Content PubMed PubMed Citation Articles by Siddegowda, Y. K. B. Articles by Mishra, S. K.

¹ Division of Pharmacology and Toxicology² Division of Physiology and Climatology, Indian Veterinary Research Institute, Izatnagar-243122, Uttar Pradesh, India

Cerebral ischaemia 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 chickens maintained either at 23–24°C with 55–65% humidity (control conditions) or exposed to 40 ± 1°C with 35% humidity for 4 h (heat stress). Contractions were elicited with vasoconstrictors such as 5-HT, phenylephrine, guanfacine and CaCl₂ (K⁺-depolarized) in endothelium-denuded arterial rings. Heat stress significantly increased the potency of 5-HT, but had no effect on the sensitivity of the vessel to phenylephrine or 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 (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 control conditions, but it significantly decreased the agonist potency in heat stress. Interestingly, nifedipine (1 µM) markedly inhibited 5-HT-induced contractions both in control conditions and in heat stress, implying an inhibitory effect on both Ca²⁺ influx and release. Thus, nifedipine had a markedly greater inhibitory effect on 5-HT-induced contractions in heat stress compared with control conditions. The results suggest that heat stress increased the vasoconstrictor responses to 5-HT by a mechanism that involved extracellular Ca²⁺ influx through nifedipine-sensitive L-type calcium channels.

(Received 5 June 2007; accepted after revision 23 August 2007; first published online 24 August 2007)
Corresponding author S. K. Mishra: Division of Pharmacology and Toxicology, Indian Veterinary Research Institute, Izatnagar-243122, Uttar Pradesh, India. Email: smishraivri{at}rediffmail.com