STIMULATION OF Na^+/H^+ EXCHANGE INDUCED BY ANGIOTENSIN II IN CULTURED RAT VASCULAR SMOOTH MUSCLE CELLS : ROLE OF Ca^<2+> AND C-KINASE

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Changes in cytosolic calcium concentration ([Ca^2+]i) have been implicated in the regulation of intracellular pH (pHi) in several cell types. In the present study we investigated the regulatory mechanism of Na^+/H^+ exchange induced by angiotensin II (AII) in cultured rat vascular smooth muscle cells (VSMCs). Serially passaged VSMCS from Sprague-Dawley rat thoracic aorta were grown on coverslips and loaded with the pH-sensitive fluorescent indicator 2',7'-bis (carboxyethyl)-5,6-carboxyfluorescein (BCECF). In HCO_3-free Ringer solution, pH 7.40, the resting pHi was 7.21±0.01 (n=21). A biphasic response was seen after exposure of these cells to AII: an initial transient a acidification, followed by sustained alkalization. The magnitude of alkalization was dose-dependent. AII-mediated acidification was completely inhibited by [Sar^1-Iie^5-Gly^8]AII, but amiloride had no effect. In contrast, the alkalization induced by AII was abolished by both amiloride and Na^+-free medium. In Ca^<2+>-free medium, the AII-induced alkalization was partially blocked and verapamil also caused partial inhibition. Since AII activates phospholipase C in VSMCs, we examined whether AII would increase Na^+/H^+ exchange by activation of protein kinase C. An inhibitor of protein kinase C, 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H-7), partially inhibited the alkalization induced by AII. These results indicate that AII stimulates cytoplasmic alkalization via an amiloride-sensitive Na^+/H^+ exchange system in cultured rat VSMCs, and that this AII-stimulated Na^+/H^+ exchange is mediated by Ca^<2+>-dependent and protein kinase C-dependent mechanisms.
社団法人日本循環器学会の論文
1992-02-20

STIMULATION OF Na^+/H^+ EXCHANGE INDUCED BY ANGIOTENSIN II IN CULTURED RAT VASCULAR SMOOTH MUSCLE CELLS : ROLE OF Ca^<2+> AND C-KINASE

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