酸中毒增强Ca2+激活的氯离子通道对产后早期血管张力调节的贡献

IF 2.1 Q3 PHYSIOLOGY
Anastasia A. Shvetsova , Margarita A. Khlystova , Valentina S. Shateeva , Sofia D. Simonenko , Anna A. Borzykh , Denis V. Abramochkin , Dina K. Gaynullina
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引用次数: 0

摘要

酸中毒常发生在新生儿临床并发症中,可导致动脉张力调节机制的改变。然而,目前尚不清楚酸中毒如何影响早期个体形成过程中动脉中Ca2+激活的氯离子通道(CaCC)的活性。我们假设它们的活性可能在酸中毒期间增加。方法观察成年大鼠和10-13日龄大鼠隐动脉的等长收缩。使用荧光指示剂BCECF-AM测量细胞内pH值,同时以等长模式记录动脉制剂的收缩活性。结果pH = 6.8的代谢性酸中毒使成年大鼠和10-13日龄大鼠的动脉收缩反应明显降低。在pH = 7.4和pH = 6.8时,成年大鼠动脉中没有CaCC的功能贡献。然而,在10-13日龄的大鼠幼崽中,pH = 6.8时CaCC的功能贡献高于pH = 7.4。结论在出生后早期个体发育过程中,酸中毒增强了CaCC在动脉中的功能作用,但在成年期没有。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Acidosis enhances contribution of Ca2+-activated chloride channels to vascular tone regulation in early postnatal period

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 Ca2+-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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来源期刊
CiteScore
3.20
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