期刊
MOLECULAR AND CELLULAR ENDOCRINOLOGY
卷 350, 期 1, 页码 20-30出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mce.2011.11.018
关键词
CCK receptors; Gastrin 17; Nitric oxide; Signaling
资金
- Universita del Piemonte Orientale A. Avogadro
- Regione Piemonte-Ricerca Sanitaria Finalizzata
In anesthetized pigs gastrin-17 increased coronary blood flow through CCK1/CCK2 receptors and beta(2)-adrenoceptors-related nitric oxide (NO) release. Since the intracellular pathway has not been investigated the purpose of this study was to examine in coronary endothelial cells the CCK1/CCK2 receptors-related signaling involved in the effects of gastrin-17 on NO release. Gastrin-17 caused a concentration-dependent increase of NO production (17.3-62.6%; p < 0.05), which was augmented by CCK1/CCK2 receptors agonists (p < 0.05). The effect of gastrin-17 was amplified by the adenylyl-cyclase activator and beta(2)-adrenoceptors agonist (p < 0.05), abolished by cAMP/PKA and beta(2)-adrenoceptors and CCK1/CCK2 receptors blockers, and reduced by PLC/PKC inhibitor. Finally, Western-blot revealed the preferential involvement of PKA vs. PKC as downstream effectors of CCK1/CCK2 receptors activation leading to Akt, ERK, p38 and endothelial NOS (eNOS) phosphorylation. In conclusion, in coronary endothelial cells, gastrin-17 induced eNOS-dependent NO production through CCK1/CCK2 receptors- and beta(2)-adrenoceptors-related pathway. The intracellular signaling involved a preferential PKA pathway over PKC. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
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