Effects of cigarette smoking,hypoxia and vasoactive mediators on the production of PGI2 and TXA2 in cultured pulmonary artery endothelial cells |
| |
Authors: | Su Yun-chao Wang Di-xun |
| |
Institution: | (1) Department of Pathophysiology, Tongji Medical University, Wuhan |
| |
Abstract: | Summary Effects of cigarette smoke extract (CSE) and some vasoactive mediators on the production of PGI2 and TXA2 in normoxic and hypoxic pulmonary artery endothelial cells (PAECs) in culture were studied. The production of PGI2 in PAECs was inhibited by hypoxia or verapamil, but promoted by angiotensin II (A II), noradrenaline (NE) or platelet activating
factor (PAF), while that of TXA2 slightly increased except when treated with PAF. The effect of A II, NE, PAF and verapamil, however, was not influenced by
hypoxia. CSE inhibited the production of PGI2 in normoxic PAECs but did not further reduce 6-keto-PGF1α in hypoxic PAECs medium. The results suggested that a) the production of PGI2 during hypoxia might be stimulated by vasoactive mediators produced during hypoxia, not by hypoxia directly; b) the production
and release of PGI, were related to intracellular calcium, c) the augmented production of PGI2 might be one of the mechanisms in the pulmonary vasodilating role of PAF: and d) prostaglandin production might be associated
with the alteration of hypoxic pulmonary vasoreactivity after cigarette smoking. |
| |
Keywords: | hypoxia smoking prostaglandins pulmonary circulation vascular endothelium |
本文献已被 SpringerLink 等数据库收录! |
|