期刊
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
卷 284, 期 6, 页码 L1121-L1126出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajplung.00422.2002
关键词
pulmonary circulation; arteries; hypoxia
The main aim of this study was to determine the effects of endothelium removal on tension and intracellular Ca2+ ([Ca2+](i)) during hypoxic pulmonary vasoconstriction (HPV) in rat isolated intrapulmonary arteries ( IPA). Rat IPA and mesenteric arteries (MA) were mounted on myographs and loaded with the Ca2+-sensitive fluorophore fura PE-3. Arteries were precontracted with prostaglandin F-2alpha, and the effects of hypoxia were examined. HPV in isolated IPA consisted of a transient constriction superimposed on a second sustained phase. Only the latter phase was abolished by endothelial denudation. However, removal of the endothelium had no effect on [Ca2+](i) at any point during HPV. The endothelin-1 antagonists BQ-123 and BQ-788 did not affect HPV, although constriction induced by 100 nM endothelin-1 was abolished. In MA, hypoxia induced an initial transient rise in tension and [Ca2+](i), followed by vasodilatation and a fall in [Ca2+](i) to (but not below) prehypoxic levels. These results are consistent with sustained HPV being mediated by an endothelium-derived constrictor factor that is distinct from endothelin-1 and that elicits vasoconstriction via Ca2+ sensitization.
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