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Am J Physiol Cell Physiol 279: C1540-C1549, 2000;
0363-6143/00 $5.00
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Vol. 279, Issue 5, C1540-C1549, November 2000

Sustained membrane depolarization and pulmonary artery smooth muscle cell proliferation

Oleksandr Platoshyn1, Vera A. Golovina2, Colleen L. Bailey1, Alisa Limsuwan1, Stefanie Krick1, Magdalena Juhaszova3, Jan E. Seiden2, Lewis J. Rubin1, and Jason X.-J. Yuan1

1 Department of Medicine, University of California School of Medicine, San Diego, California 92103-8382; 2 Departments of Physiology and Medicine, University of Maryland, Baltimore 21201; and 3 National Institute on Aging, Gerontology Research Center, Baltimore, Maryland 21224

Pulmonary vasoconstriction and vascular medial hypertrophy greatly contribute to the elevated pulmonary vascular resistance in patients with pulmonary hypertension. A rise in cytosolic free Ca2+ ([Ca2+]cyt) in pulmonary artery smooth muscle cells (PASMC) triggers vasoconstriction and stimulates cell growth. Membrane potential (Em) regulates [Ca2+]cyt by governing Ca2+ influx through voltage-dependent Ca2+ channels. Thus intracellular Ca2+ may serve as a shared signal transduction element that leads to pulmonary vasoconstriction and vascular remodeling. In PASMC, activity of voltage-gated K+ (Kv) channels regulates resting Em. In this study, we investigated whether changes of Kv currents [IK(V)], Em, and [Ca2+]cyt affect cell growth by comparing these parameters in proliferating and growth-arrested PASMC. Serum deprivation induced growth arrest of PASMC, whereas chelation of extracellular Ca2+ abolished PASMC growth. Resting [Ca2+]cyt was significantly higher, and resting Em was more depolarized, in proliferating PASMC than in growth-arrested cells. Consistently, whole cell IK(V) was significantly attenuated in PASMC during proliferation. Furthermore, Em depolarization significantly increased resting [Ca2+]cyt and augmented agonist-mediated rises in [Ca2+]cyt in the absence of extracellular Ca2+. These results demonstrate that reduced IK(V), depolarized Em, and elevated [Ca2+]cyt may play a critical role in stimulating PASMC proliferation. Pulmonary vascular medial hypertrophy in patients with pulmonary hypertension may be partly caused by a membrane depolarization-mediated increase in [Ca2+]cyt in PASMC.

intracellular calcium; voltage-gated potassium channels; membrane potential


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