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Am J Physiol Lung Cell Mol Physiol 281: L1115-L1122, 2001;
1040-0605/01 $5.00
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Vol. 281, Issue 5, L1115-L1122, November 2001

Inhibition of voltage-gated K+ currents by endothelin-1 in human pulmonary arterial myocytes

Larissa A. Shimoda, J. T. Sylvester, Gregory M. Booth, Tenille H. Shimoda, Sonya Meeker, Bradley J. Undem, and James S. K. Sham

Divisions of Pulmonary and Critical Care Medicine and Allergy and Clinical Immunology, Johns Hopkins School of Medicine, Baltimore, Maryland 21224

Recent studies demonstrate that endothelin-1 (ET-1) constricts human pulmonary arteries (PA). In this study, we examined possible mechanisms by which ET-1 might constrict human PA. In smooth muscle cells freshly isolated from these arteries, whole cell patch-clamp techniques were used to examine voltage-gated K+ (KV) currents. KV currents were isolated by addition of 100 nM charybdotoxin and were identified by current characteristics and inhibition by 4-aminopyridine (10 mM). ET-1 (10-8 M) caused significant inhibition of KV current. Staurosporine (1 nM), a protein kinase C (PKC) inhibitor, abolished the effect of ET-1. Rings of human intrapulmonary arteries (0.8-2 mm OD) were suspended in tissue baths for isometric tension recording. ET-1-induced contraction was maximal at 10-8 M, equal to that induced by KV channel inhibition with 4-aminopyridine, and attenuated by PKC inhibitors. These data suggest that ET-1 constricts human PA, possibly because of myocyte depolarization via PKC-dependent inhibition of KV. Our results are consistent with data we reported previously in the rat, suggesting similar mechanisms may be operative in both species.

lung; protein kinase C; vascular smooth muscle; pulmonary arterial smooth muscle cells


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