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Am J Physiol Lung Cell Mol Physiol 274: L552-L559, 1998;
1040-0605/98 $5.00
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Vol. 274, Issue 4, L552-L559, April 1998

Hypoxic exposure time dependently modulates endothelininduced contraction of pulmonary artery smooth muscle

Russell A. Bialecki, Carol S. Fisher, Wallace W. Murdoch, Herbert G. Barthlow, Richard B. Stow, Michael Mallamaci, and William Rumsey

Respiratory, Inflammatory, and Neurological Diseases Research Section, Zeneca Pharmaceuticals, Zeneca, Inc., Wilmington, Delaware 19850-5437

Endothelins (ETs) have been implicated in the pathogenesis of hypoxia-induced pulmonary hypertension. We determined whether hypoxic exposure of rats (10% O2-90% N2, 1 atm, 1-48 days) altered contraction to ET in isolated segments of endothelium-denuded extralobar branch pulmonary artery (PA) and aorta. Hypoxic exposure increased hematocrit, right ventricular hypertrophy, and ET-1 plasma concentration. Hypoxia also caused a sustained decrease in PA but not in aorta sensitivity to ET-1. In comparison, hypoxic exposure throughout 12 days decreased time dependently the maximum contraction of PA to ET-1, BaCl2, and KCl. The hypoxia-induced decrease in maximum contraction of PA to ET-1 returned toward normal levels by 21 days and approximated control levels by 48 days. After 14 days of hypoxia, right ventricular hypertrophy correlated with decreased sensitivity of PA to ET-1. After 21 days of hypoxia, PA sensitivity to ET-2 and ET-3 was decreased, and sarafotoxin S6c-induced contraction was abolished. In conclusion, hypoxic exposure time dependently modulates the responsiveness of PA smooth muscle to ETs, BaCl2, and KCl. The hypoxia-induced changes in tissue responsiveness to ET-1 may be associated with increased plasma concentrations of this peptide.

aorta; hypoxia; sarafotoxin S6b; sarafotoxin S6c; pulmonary hypertension


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