VA Medical Center, 1 Veterans Drive, 111C, Minneapolis, MN, 55417, USA.
Adv Exp Med Biol. 2010;661:3-14. doi: 10.1007/978-1-60761-500-2_1.
Hypoxic pulmonary vasoconstriction (HPV) is an important mechanism by which localized flow of blood in small resistance pulmonary arteries is matched to alveolar ventilation. This chapter discusses the role of several potassium and calcium channels in HPV, both in enhancing calcium influx into smooth muscle cells (SMCs) and in stimulating the release of calcium from the sarcoplasmic reticulum, thus increasing cytosolic calcium. The increase in calcium sensitivity caused by hypoxia is reviewed in Chapter 19. Particular attention is paid to the activity of the L-type calcium channels which increase calcium influx as a result of membrane depolarization and also increase calcium influx at any given membrane potential in response to hypoxia. In addition, activation of the L-type calcium channel may, in the absence of any calcium influx, cause calcium release from the sarcoplasmic reticulum. Many of these mechanisms have been reported to be involved in both HPV and in normoxic contraction of the ductus arteriosus.
低氧性肺血管收缩（HPV）是一种重要的机制，通过该机制，小阻力肺动脉中的局部血流与肺泡通气相匹配。本章讨论了几种钾和钙通道在 HPV 中的作用，包括增强平滑肌细胞（SMCs）内钙内流和刺激肌浆网释放钙，从而增加细胞浆内钙。第 19 章综述了低氧引起的钙敏感性增加。特别关注 L 型钙通道的活性，该通道通过膜去极化增加钙内流，并且在低氧条件下响应于任何给定的膜电位增加钙内流。此外，L 型钙通道的激活即使没有任何钙内流也可能导致肌浆网内钙释放。许多这些机制已被报道参与 HPV 和正常氧合的动脉导管收缩。
