Uzun, ÖzgeDemiryürek, Abdullah T.2020-04-302020-04-3020060031-7012https://doi.org/10.1159/000093521https://hdl.handle.net/20.500.12684/4441Demiryurek, Abdullah/0000-0003-4762-4745WOS: 000239244100003PubMed: 16717478The aim of this study was to investigate the effect of hypoxia on and the role of nitric oxide (NO) and cyclooxgenase inhibition in hypoxia-induced vasoconstriction in sheep isolated pulmonary veins. We used the potent pulmonary vasoconstrictor U46619, a thromboxane analog, as a precontractile agent. Our results showed that hypoxia caused a vasoconstriction both under resting tone and in U46619 (10(-6) mol/l) precontracted pulmonary veins. In the presence of the nonselective NO synthase inhibitior N omega-nitro-L-arginine methyl ester (L-NAME; 3 x 10(-5) mol/l), the hypoxic pulmonary vasoconstriction (HPV) was significantly increased in veins under resting force. However, there was a decrease in HPV in pulmonaryveins precontracted with U46619 in the presence of L-NAME. Moreover, L-NAME markedly augmented the U46619-induced pulmonary contractions under normoxic conditions. Cyclooxygenase inhibition with indomethacin (10(-5) mol/l) significantly reduced the HPV both under resting tone and in precontracted veins. Indomethacin also significantly decreased the U46619-induced pulmonary contractions prior to the induction of hypoxia. Our findings suggest that NO and prostaglandins can act as a modulators of the hypoxic vasoconstriction in isolated pulmonary veins. Copyright (c) 2006 S. Karger AG, Basel.en10.1159/000093521info:eu-repo/semantics/closedAccesshypoxiapulmonary veinsN omega-nitro-L-arginine methyl esterindomethacinArticle773122129WOS:000239244100003Q3