Koh E, Morimoto S, Kim S, Nabata T, Miyashita Y, Ogihara T
Department of Geriatric Medicine, Osaka University Medical School, Japan.
Biochem Int. 1990;20(2):375-80.
The effect of endothelin (ET) on the intracellular pH (pHi) of vascular smooth muscle cells (VSMC), was investigated using a fluorescent pH indicator 2',7'-bis(carboxyethyl)carboxyfluorescein (BCECF). ET at concentrations of over 10(-9) M caused dose-dependent transient acidification followed by Na(+)-dependent and amiloride-sensitive alkalization of the cells due to stimulation of Na+/H+ exchange. The alkalization induced by ET was Ca2(+)-dependent and was inhibited by a calcium channel blocker, nicardipine. Pretreatment with H-7, an inhibitor of protein kinase C, also inhibited the ET-induced cell alkalization. These results indicate that ET stimulates Na+/H+ exchange, resulting in alkalization of VSMC and that this ET-induced cell-alkalization is probably linked to Ca2+ influx and activation of protein kinase C.
利用荧光pH指示剂2'，7'-双（羧乙基）羧基荧光素（BCECF）研究了内皮素（ET）对血管平滑肌细胞（VSMC）细胞内pH值（pHi）的影响。浓度超过10^(-9) M的ET会引起剂量依赖性的短暂酸化，随后由于Na+/H+交换的刺激，细胞出现依赖Na+且对氨氯地平敏感的碱化。ET诱导的碱化依赖于Ca2+，并被钙通道阻滞剂尼卡地平抑制。用蛋白激酶C抑制剂H-7预处理也能抑制ET诱导的细胞碱化。这些结果表明，ET刺激Na+/H+交换，导致VSMC碱化，并且这种ET诱导的细胞碱化可能与Ca2+内流和蛋白激酶C的激活有关。
