| REVIEW ARTICLE |
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| Year : 2011 | Volume
: 1
| Issue : 1 | Page : 48-71 |
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Functional ion channels in human pulmonary artery smooth muscle cells: Voltage-dependent cation channels
Amy L Firth1, Carmelle V Remillard2, Oleksandr Platoshyn2, Ivana Fantozzi2, Eun A Ko3, Jason X J. Yuan4
1 The Salk Institute for Biological Studies, La Jolla, California, USA
2 Department of Medicine, University of California, San Diego, La Jolla, California, USA
3 Department of Medicine (Section of Pulmonary, Critical Care, Sleep and Allergy), Institute for Personalized Respiratory Medicine, University of Illinois at Chicago, Chicago, Illinois, USA
4 Department of Medicine, University of California, San Diego, La Jolla, California;Department of Medicine (Section of Pulmonary, Critical Care, Sleep and Allergy), Institute for Personalized Respiratory Medicine, University of Illinois at Chicago, Chicago, Illinois, USA
Correspondence Address:
Jason X J. Yuan
Department of Medicine (Section of Pulmonary, Critical Care and Sleep and Allergy), Institute for Personalized Respiratory Medicine, University of Illinois at Chicago, COMRB Rm. 3131 (MC 719), 909 South Wolcott Avenue, Chicago, Illinois 60612
USA
DOI: 10.4103/2045-8932.78103 PMID: 21927714
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The activity of voltage-gated ion channels is critical for the maintenance of cellular membrane potential and generation of action potentials. In turn, membrane potential regulates cellular ion homeostasis, triggering the opening and closing of ion channels in the plasma membrane and, thus, enabling ion transport across the membrane. Such transmembrane ion fluxes are important for excitation-contraction coupling in pulmonary artery smooth muscle cells (PASMC). Families of voltage-dependent cation channels known to be present in PASMC include voltage-gated K + (Kv) channels, voltage-dependent Ca 2+ -activated K + (Kca) channels, L- and T- type voltage-dependent Ca 2+ channels, voltage-gated Na + channels and voltage-gated proton channels. When cells are dialyzed with Ca 2+ -free K + - solutions, depolarization elicits four components of 4-aminopyridine (4-AP)-sensitive Kvcurrents based on the kinetics of current activation and inactivation. In cell-attached membrane patches, depolarization elicits a wide range of single-channel K + currents, with conductances ranging between 6 and 290 pS. Macroscopic 4-AP-sensitive Kv currents and iberiotoxin-sensitive Kca currents are also observed. Transcripts of (a) two Na + channel α-subunit genes (SCN5A and SCN6A), (b) six Ca2+ channel α−subunit genes (α1A, α 1Β , α 1Χ , α1D, α1E and α1G) and many regulatory subunits (α2δ1, β1-4, and γ6), (c) 22 Kv channel α−subunit genes (Kv1.1 - Kv1.7, Kv1.10, Kv2.1, Kv3.1, Kv3.3, Kv3.4, Kv4.1, Kv4.2, Kv5.1, Kv 6.1-Kv6.3, Kv9.1, Kv9.3, Kv10.1 and Kv11.1) and three Kv channel β-subunit genes (Kvβ1-3) and (d) four Kca channel α−subunit genes (Sloα1 and SK2-SK4) and four Kca channel β-subunit genes (Kcaβ1-4) have been detected in PASMC. Tetrodotoxin-sensitive and rapidly inactivating Na + currents have been recorded with properties similar to those in cardiac myocytes. In the presence of 20 mM external Ca 2+ , membrane depolarization from a holding potential of -100 mV elicits a rapidly inactivating T-type Ca 2+ current, while depolarization from a holding potential of -70 mV elicits a slowly inactivating dihydropyridine-sensitive L-type Ca 2+ current. This review will focus on describing the electrophysiological properties and molecular identities of these voltage-dependent cation channels in PASMC and their contribution to the regulation of pulmonary vascular function and its potential role in the pathogenesis of pulmonary vascular disease. |
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