Tristani-Firouzi M, Reeve H L, Tolarova S, Weir E K, Archer S L
Department of Pediatrics, University of Minnesota, Minneapolis 55455, USA.
J Clin Invest. 1996 Nov 1;98(9):1959-65. doi: 10.1172/JCI118999.
The ductus arteriosus is a vital fetal structure allowing blood ejected from the right ventricle to bypass the pulmonary circulation in utero. Closure of the ductus arteriosus at birth, essential for postnatal adaptation, is initiated by an increase in oxygen (O2) tension. We recently demonstrated the presence of O2-sensitive potassium channels in the fetal and adult pulmonary circulation which regulate vascular tone in response to changes in O2 tension. In this study, we assessed the cellular mechanisms underlying O2-induced constriction of the ductus arteriosus in late-gestation fetal rabbits. We report that O2 reversibly inhibits a 58-pS voltage- and 4-aminopyridine-sensitive potassium channel, causing membrane depolarization, an increase in intracellular calcium through L-type voltage-gated calcium channels, and constriction of the ductus arteriosus. We conclude that the effector mechanism for O2 sensing in the ductus arteriosus involves the coordinated action of delayed rectifier potassium channels and voltage-gated calcium channels.
动脉导管是胎儿期的一个重要结构，它使右心室射出的血液在子宫内绕过肺循环。出生时动脉导管的关闭对出生后的适应至关重要，它是由氧（O2）张力增加引发的。我们最近证明了胎儿和成人肺循环中存在对氧敏感的钾通道，这些通道可根据氧张力的变化调节血管张力。在本研究中，我们评估了妊娠晚期胎儿兔动脉导管中氧诱导收缩的细胞机制。我们报告，氧可逆性抑制一种58皮秒的电压和4-氨基吡啶敏感的钾通道，导致膜去极化，通过L型电压门控钙通道使细胞内钙增加，从而引起动脉导管收缩。我们得出结论，动脉导管中氧感知的效应机制涉及延迟整流钾通道和电压门控钙通道的协同作用。
