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1 Service de Physiologie-Explorations Fonctionnelles, Centre Hospitalier Universitaire Cochin, Assistance Publique, Hopitaux de Paris, Universite Paris 5, 75014 Paris, France
2 Laboratoire d'Immunologie Biologique, Faculte de Medecine Cochin, Universite Paris 5, 75014 Paris, France
3 Unite 408, Institut National de la Sante et de la Recherche Medicale, 75018 Paris, France
4 Service de Reanimation Pediatrique, Hopital Robert Debre, Assistance Publique, Hopitaux de Paris, 75019 Paris, France
* To whom correspondence should be addressed. E-mail: anh-tuan.dinh-xuan{at}cch.ap-hop-paris.fr.
Nitric oxide (NO) is synthesized from L-arginine by Ca2+/calmodulin-sensitive endothelial NO synthase type III isoform (eNOS). The present study assesses the role of Ca2+/calmodulin-dependent protein kinase II (CaMK II) in endothelium-dependent relaxation and NO synthesis. The effects of three CaMK II inhibitors were investigated in endothelium-intact aortic rings of normotensive rats. NO synthesis was assessed by NO sensor and chemiluminescence in culture medium of cultured porcine aortic endothelial cells stimulated with the Ca2+ ionophore A23187 and thapsigargin. Rat aortic endothelial NOS activity was measured by the conversion of [3H]L-arginine to [3H]L-citrulline. Three CaMK II inhibitors, polypeptide 281-302, KN-93 and lavendustin C, attenuated endothelium-dependent relaxation of endothelium-intact aortic rings in response to acetylcholine, A23187, and thapsigargin. None of the CaMK II inhibitors affected relaxation induced by NO donors. In porcine aortic endothelial cell line, KN-93 decreased NO synthesis and caused a rightward shift of the concentration-response curves to A23187 and thapsigargin. In rat aortic endothelial cells, KN-93 significantly decreased bradykinin-induced eNOS activity. These results suggest that CaMK II was involved in NO synthesis as a result of Ca2+-dependent activation of eNOS.
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