The role of ion channels in hypoxic pulmonary vasoconstriction

• Published in: Advances in experimental medicine and biology Vol. 661; p. 3
• Main Authors: Weir, E Kenneth, Cabrera, Jésus A, Mahapatra, Saswati, Peterson, Douglas A, Hong, Zhigang
• Format: Journal Article
• Language: English
• Published: United States 2010
• Subjects: Animals; Calcium - metabolism; Ductus Arteriosus - metabolism; Humans; Hypoxia - metabolism; Ion Channels - metabolism; Lung - blood supply; Lung - metabolism; Muscle Contraction - physiology; Myocytes, Smooth Muscle - cytology; Myocytes, Smooth Muscle - metabolism; Oxygen - metabolism; Pulmonary Artery - cytology; Pulmonary Artery - metabolism; Pulmonary Circulation - physiology; Vasoconstriction - physiology
• ISSN: 0065-2598
• 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.