作者: Wenze Wang , Li Pang , Philip Palade
DOI: 10.1159/000318776
关键词:
摘要: Background: We previously reported that angiotensin II caused an endothelial-dependent increase in L-type voltage-dependent Ca2+ channel (CaV1.2) cultured arteries, but the signaling pathways are not clear. Methods: Endothelial damage was generated by brief intra-arterial perfusion with 0.3% CHAPS. CaV1.2 expression, function and H2O2 were measured Western blot, tension recording Amplex Red assay kit, respectively. Results: Angiotensin dose-dependently upregulated expression endothelium-intact arteries. The upregulation of arteries blocked NAD(P)H oxidase inhibitor diphenyleneiodonium (DPI), apocynin, a more specific gp91ds-tat also catalase. similarly endothelium-damaged latter effect DPI apocynin. increased production this catalase gp91ds-tat. is accompanied response to KCl activator FPL 64176, attenuated Conclusion: These results suggest stimulates endothelial oxidase-produced H2O2, which may additionally act through vascular smooth muscle oxidase, upregulate protein.