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1 Department of Physiology and Pharmacology, Institute of Comparative Medicine, The University of Georgia, Athens, GA, USA
2 Department of Respiratory Medicine and Allergy, King's College London, London, United Kingdom
* To whom correspondence should be addressed. E-mail: troberts{at}vet.uga.edu.
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 pre-contracted with prostaglandin F2
, and the effects of hypoxia examined. HPV in isolated IPA consisted of a transient constriction superimposed upon a second sustained phase. Only the latter phase was abolished by endothelial denudation. However, removal of the endothelium had no effect upon [Ca2+]i at any point during HPV. The endothelin-1 antagonists, BQ123 and BQ788, did not affect upon 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) pre-hypoxic 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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