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Articles in PresS, published online ahead of print April 18, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00789.2001
Submitted on September 6, 2001
Accepted on April 8, 2002
1 Service de Physiologie-Explorations Fonctionnelles, CHU Cochin Port-Royal, AP-HP-Universite Paris 5, Paris, France
2 Service d'Immunologie Biologique, CHU Cochin Port-Royal, AP-HP-Universite Paris 5, Paris, France
3 Service de Reanimation Pediatrique, Hopital Robert Debre, Paris, France
* To whom correspondence should be addressed. E-mail: anh-tuan.dinh-xuan{at}cch-hop-paris.fr.
The endothelial nitric oxide synthase (eNOS) isoform is controlled by Ca2+-calmodulin and caveolin 1 in caveolae. It has been recently suggested that the Na+/Ca2+ exchanger (NCX), also expressed in endothelial caveolae, was involved in eNOS activation. To investigate the role played by NCX in nitric oxide (NO) synthesis, we have assessed the effects of Na+ loading (induced by monensin) on rat aortic rings and cultured porcine aortic endothelial cells. Effect of monensin was evaluated by endothelium-dependent relaxation of rat aortic rings in response to acetylcholine and by real-time measurement of NO release in A23187 or bradykinin-stimulated cultured endothelial cells. Our results indicate that Na+ loading shifted to the left the acetylcholine concentration-response curve. These effects were prevented by pretreatment with the NCX inhibitor, benzamil and KB-R7943. Monensin potentiated the Ca2+-dependent NO release in cultured endothelial cells, while benzamil and KB-R7943 totally blocked the Na+ loading-induced NO release. These findings confirm the key role of NCX in reverse mode on Ca2+-dependent NO production and endothelium-dependent relaxation.
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