Acidosis enhances contribution of Ca(2+)-activated chloride channels to vascular tone regulation in early postnatal period

酸中毒增强了Ca(2+)激活氯离子通道在出生后早期对血管张力调节的作用

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Abstract

INTRODUCTION: Acidosis often occurs during clinical complications in newborns and can lead to changes in the mechanisms of arterial tone regulation. However, it is unknown how acidosis affects the activity of Ca(2+)-activated chloride channels (CaCC) in arteries during early ontogenesis. We hypothesized that their activity may increase during acidosis. METHODS: We studied isometric contractions of saphenous arteries isolated from adult and 10-13-day-old rats. Intracellular pH was measured using a fluorescent indicator BCECF-AM simultaneously with recording the contractile activity of the arterial preparation in isometric mode. RESULTS: Metabolic acidosis with pH = 6.8 caused a significant decrease in the arterial contractile responses of adult and 10-13-day-old rats. The functional contribution of CaCC was absent in the adult rat arteries both at pH = 7.4 and pH = 6.8. However, in 10-13-day-old rat pups, the functional contribution of CaCC was higher at pH = 6.8 compared to pH = 7.4. CONCLUSION: Acidosis augments the functional role of CaCC in arteries during early postnatal ontogenesis, but not in adulthood.

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