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1 Laboratoire de Physiologie Cellulaire Respiratoire, INSERM E356, Bordeaux, France
* To whom correspondence should be addressed. E-mail: christelle.guibert{at}u-bordeaux2.fr.
5-hydroxytryptamine (5-HT) is a potent pulmonary vasoconstrictor and contributes to hypoxic pulmonary vasoconstriction (HPV) and pulmonary arterial hypertension (PAH). Small intrapulmonary vessels are very sensitive to hypoxia and play a major role for blood flow regulation in the lung. Thus, we have investigated the mechanisms involved in the calcium signal to 5-HT in rat small intrapulmonary artery (IPA). Effects of 5-HT were examined in isolated IPA (external diameter < 250 µm) from rat. Digital imaging with fura-PE3 was used to record intracellular calcium concentration ([Ca2+]i) and to follow external diameter of the vessels. 5-HT induced a sustained [Ca2+]i variation which was sensitive to the inhibitor of the 5-HT2A receptors, ketanserin, and insensitive to voltage-dependent L-type calcium channel blockers (nitrendipine and nicardipine) or voltage-independent calcium channels antagonists (LOE 908, SKF 96365 and gadolinium 10 µM). The calcium response to 5-HT was also not modified by a sarcoplasmic reticulum Ca2+-ATPase inhibitor (cyclopiazonic acid, CPA) which depletes intracellular calcium store. CPA alone activated a capacitative calcium channel which was sensitive to LOE 908 and insensitive to SKF 96365 and gadolinium. The sustained calcium signal to 5- HT was partly blocked by inhibitors of arachidonic acid production (RHC 80267 and isotetrandrine) and mimicked by application of exogenous arachidonic acid. These results suggest that activation of a non- capacitative arachidonic acid sensitive receptor-operated calcium channel contributes to 5-HT-induced sustained calcium increase in small IPA.
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