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Effects of Angiotensin II on CaV1.2 Expression in Mesenteric Artery
Author(s) -
Wang Wenze,
Palade Philip
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.912.29
Subject(s) - chelerythrine , downregulation and upregulation , apocynin , cav1.2 , angiotensin ii , chemistry , nadph oxidase , protein kinase c , nad(p)h oxidase , endocrinology , vascular smooth muscle , medicine , biology , kinase , calcium channel , calcium , reactive oxygen species , biochemistry , receptor , smooth muscle , gene
Effects of angiotensin II (Ang II) on CaV1.2 L‐type calcium channel expression in 24 h cultured mesenteric arteries (MA) of Sprague‐Dawley rats were studied using Western blot, real‐time RT‐PCR and blood vessel tension recording. Ang II dose‐dependently upregulated expression of CaV1.2 protein but not its mRNA. Ang II still increased CaV1.2 expression with protein synthesis inhibited by puromycin. The upregulation of CaV1.2 expression by Ang II was blocked by protein kinase C (PKC) inhibitor chelerythrine, by NAD(P)H oxidase inhibitors diphenyleneiodonium (DPI) or apocynin, or by endothelial damage by brief perfusion with 0.3% CHAPS. The Ang II upregulation of CaV1.2 expression was blocked by catalase, and H2O2 dose‐dependently upregulated CaV1.2. After endothelial damage, H2O2 still upregulated CaV1.2 expression and this effect was inhibited by the PI3 kinase inhibitor wortmannin. MA cultured in Ang II displayed increased tension in response to CaV1.2 channel agonist FPL 64176. These results suggest that: (1) decreased degradation of CaV1.2 channel protein may contribute to Ang II‐induced upregulation of CaV1.2 expression, (2) Ang II activation of PKC, NAD(P)H oxidase and H2O2 production in the endothelium and H2O2 activation of PI3 kinase in the vascular smooth muscle mediate the upregulation, and (3) the upregulation of CaV1.2 protein contributes to increased vascular tone. Supported by HL 63903.