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1 Department of Physiology and Pharmacology, Institute of Comparative Medicine, University of Georgia, Athens, Georgia 30602-7389; and 2 Department of Asthma, Allergy, and Respiratory Science, Guy's King's and St. Thomas' School of Medicine, King's College London, London SE1 9RT, United Kingdom
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 F2
, 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.
pulmonary circulation; arteries; hypoxia
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