Uzun Ozge, Demiryürek A Tuncay, Kanzik Ilker
Department of Pharmacology, Abant Izzet Baysal University, Faculty of Medicine, Düzce, Turkey.
Pharmacology. 2002 Apr;64(4):214-6. doi: 10.1159/000056174.
The introduction of hypoxia is well known to cause contraction of pulmonary artery rings in vitro. Despite intensive studies, the cellular mechanisms of hypoxic pulmonary vasoconstriction are still not well defined. In this study, we aimed to determine the contribution of G(S) proteins in hypoxia-induced vasoconstriction in large-diameter sheep pulmonary arteries using cholera toxin (CT). Hypoxia caused further contractions in serotonin but not in NaF-precontracted pulmonary artery rings. However, hypoxic vasoconstriction due to lowering of pO(2) from 97 to 5 mm Hg was totally abolished by preincubation with CT in serotonin-precontracted arteries. These preliminary results indicate that signal transduction mediated by G(s) proteins may be an important mechanism in the hypoxic vasoconstriction of isolated pulmonary arteries of sheep.
众所周知,在体外引入低氧会导致肺动脉环收缩。尽管进行了深入研究,但低氧性肺血管收缩的细胞机制仍未完全明确。在本研究中,我们旨在使用霍乱毒素(CT)来确定G(S)蛋白在大直径绵羊肺动脉低氧诱导的血管收缩中的作用。低氧使血清素预收缩的肺动脉环进一步收缩,但对氟化钠预收缩的肺动脉环无此作用。然而,在血清素预收缩的动脉中,预先用CT孵育可完全消除因pO(2)从97 mmHg降至5 mmHg而导致的低氧性血管收缩。这些初步结果表明,由G(s)蛋白介导的信号转导可能是绵羊离体肺动脉低氧性血管收缩的重要机制。