Diverse effects of prostaglandin E2 on vascular contractility

Prostaglandin E-2 (PGE(2)) is a major prostanoid produced under inflammatory situations. There have been controversial reports showing contractile or relaxant effect of PGE(2) on vascular tone in various types of blood vessels. Thus, it is still elusive whether and how PGE(2) modulates vascular tone. We here assessed the effects of PGE(2) on vascular contractility using different types of vasculatures isolated form rat. In endothelium-denuded aortas and mesenteric arteries, PGE(2) (1 nM-10 mu M) concentration-dependently enhanced the contraction elicited by K+ (35.4 mM) or norepinephrine (10 nM). In pulmonary arteries, PGE(2) did not alter the both-induced contraction. Tail arteries were relaxed by a low dose of PGE(2) (1-100 nM), but this response shifted to contraction by the higher dose of PGE(2) (300 nM-10 mu M). There are four types of PGE(2) receptors EP1-4. RT-PCR showed that aortas and mesenteric arteries abundantly expressed EP3, while tail arteries abundantly expressed EP4. We next revealed that selective EP3 agonism enhanced the contraction in mesenteric arteries, whereas EP4 agonism induced relaxation in tail arteries. Taken together, PGE(2) causes different contractile responses depending on the type of vascular bed. This phenomenon may be due to the difference in expression pattern and activity of EP receptors.