Abstract
The effects of hypoxia on endothelin-1 (ET-1) release were studied in vitro in human, sheep (under resting force) and preconstricted rabbit pulmonary artery rings. Hypoxic contraction in human and sheep arteries was well maintained, while that in rabbit arteries was transient and followed by vasorelaxation. The basal production of ET-1, measured by radioimmunoassay in Krebs solution, was not affected by hypoxia in human pulmonary arteries (control, 0.71 ±0.16 vs hypoxia, 0.73 ± 0.41 fmol ml−1 20 min−1). Similarly, hypoxia did not produce any change in the levels of ET-1 released by sheep pulmonary artery rings. In the latter preparation, the role of hypoxia in ET-1 release was characterized in either the early or the late phase of the contraction, and no significant change was observed (control, 26.52±6.36, hypoxia early phase, 19.06±5.82 and hypoxia late phase, 26.4±9.03 fmol ml−115 min−1). In rabbit pulmonary arteries hypoxia also failed to stimulate ET-1 release (control, 2.28±0.85, hypoxia, 5.95±3.27 fmol ml−115 min−1). Basal ET-1 release can be seen to be significantly greater in sheep than in human pulmonary artery rings under oxygenated conditions. These results suggest that ET-1 is not the mediator regulating pulmonary artery contraction during acute hypoxia.