Effects of cigarette smoking, hypoxia and vasoactive mediators on the production of PGI₂ and TXA₂ in cultured pulmonary artery endothelial cells

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-PGF_1α 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.