AJP - Heart and Circulatory Physiology, Vol 242, Issue 5 907-H915, Copyright © 1982 by American Physiological Society

ARTICLES

Membrane properties of smooth muscle cells in pulmonary hypertensive rats

H. Suzuki and B. M. Twarog

The membrane properties of smooth muscle cells in rat main pulmonary artery (MPA) and small pulmonary artery (SPA) were investigated during chronic normobaric hypoxia and after monocrotaline injection. As chronic pulmonary hypertension developed, pronounced differences between MPA and SPA were observed. These findings may shed light on mechanisms of smooth muscle hypertrophy. 1) The resting membrane potential of smooth muscle in MPA became less negative than the normal (depolarized), whereas the resting membrane potential of smooth muscle in SPA became more negative (hyperpolarized). 2) In MPA, both the length and time constants diminished. 3) In MPA, the maximum membrane depolarization produced by a 10-fold increase in extracellular [K+] decreased. 4) In SPA, the depolarization observed in K+-free solution was more rapid and greater in amplitude, and the transient hyperpolarization following restoration of K+-containing solution increased. 5) In SPA, initial and sustained depolarization evoked by Na+-deficient solutions were increased. 6) Depolarization in MPA was due to increased membrane permeability, perhaps to Cl-, whereas hyperpolarization in SPA could be attributed to increased activity of an electrogenic Na+-K+ pump.

This article has been cited by other articles:

				C. D. Fike, M. R. Kaplowitz, Y. Zhang, and J. A. Madden Voltage-gated K+ channels at an early stage of chronic hypoxia-induced pulmonary hypertension in newborn piglets Am J Physiol Lung Cell Mol Physiol, December 1, 2006; 291(6): L1169 - L1176. [Abstract] [Full Text] [PDF]

				J. Wang, L. Weigand, W. Wang, J. T. Sylvester, and L. A. Shimoda Chronic hypoxia inhibits Kv channel gene expression in rat distal pulmonary artery Am J Physiol Lung Cell Mol Physiol, June 1, 2005; 288(6): L1049 - L1058. [Abstract] [Full Text] [PDF]

				U. Raj and L. Shimoda Oxygen-dependent signaling in pulmonary vascular smooth muscle Am J Physiol Lung Cell Mol Physiol, October 1, 2002; 283(4): L671 - L677. [Abstract] [Full Text] [PDF]

				L. A. Shimoda, D. J. Manalo, J. S. K. Sham, G. L. Semenza, and J. T. Sylvester Partial HIF-1{alpha} deficiency impairs pulmonary arterial myocyte electrophysiological responses to hypoxia Am J Physiol Lung Cell Mol Physiol, July 1, 2001; 281(1): L202 - L208. [Abstract] [Full Text] [PDF]

				L. A. Shimoda, J. S. K. Sham, T. H. Shimoda, and J. T. Sylvester L-type Ca2+ channels, resting [Ca2+]i, and ET-1-induced responses in chronically hypoxic pulmonary myocytes Am J Physiol Lung Cell Mol Physiol, November 1, 2000; 279(5): L884 - L894. [Abstract] [Full Text] [PDF]

				K. M. Ito, M. Sato, K. Ushijima, M. Nakai, and K. Ito Alterations of endothelium and smooth muscle function in monocrotaline-induced pulmonary hypertensive arteries Am J Physiol Heart Circ Physiol, October 1, 2000; 279(4): H1786 - H1795. [Abstract] [Full Text] [PDF]

				L. A. Shimoda, J. T. Sylvester, and J. S. K. Sham Chronic hypoxia alters effects of endothelin and angiotensin on K+ currents in pulmonary arterial myocytes Am J Physiol Lung Cell Mol Physiol, September 1, 1999; 277(3): L431 - L439. [Abstract] [Full Text] [PDF]

				K.-X. Li, B. Fouty, I. F. McMurtry, and D. M. Rodman Enhanced ETA-receptor-mediated inhibition of Kv channels in hypoxic hypertensive rat pulmonary artery myocytes Am J Physiol Heart Circ Physiol, July 1, 1999; 277(1): H363 - H370. [Abstract] [Full Text] [PDF]

				R. M. Priest, T. P. Robertson, R. M. Leach, and J. P. T. Ward Membrane Potential-Dependent and -Independent Vasodilation in Small Pulmonary Arteries from Chronically Hypoxic Rats J. Pharmacol. Exp. Ther., June 1, 1998; 285(3): 975 - 982. [Abstract] [Full Text]

				B. Fouty, P. Komalavilas, M. Muramatsu, A. Cohen, I. F. McMurtry, T. M. Lincoln, and D. M. Rodman Protein kinase G is not essential to NO-cGMP modulation of basal tone in rat pulmonary circulation Am J Physiol Heart Circ Physiol, February 1, 1998; 274(2): H672 - H678. [Abstract] [Full Text] [PDF]