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

Abstract

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 AII, 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-PGF1 alpha in hypoxic PAECs medium. The results suggest 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 PGI2 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.

Piper sarmentosum Roxb. Attenuates Vascular Endothelial Dysfunction in Nicotine-Induced Rats

“…The endothelium secretes various vasoactive substances that move to the underlying VSMC to induce vasoconstriction or vasorelaxation (Wright et al, 2004). Nicotine stimulates the release of the vasoconstrictor, endothelin-1, and inhibits the synthesis of the vasorelaxants, nitric oxide (NO) and prostacyclin, from the endothelium (Su and Wang, 1991;Toda and Toda, 2010;Durand and Gutterman, 2013). As for the endothelium-independent mechanisms, nicotine promotes vasoconstriction by activating voltage-gated potassium channels and enhancing VSMC response to norepinephrine (Mayhan and Sharpe, 2002;Olfert et al, 2018).…”