butaprost and Migraine-Disorders

Migraine pain is thought to involve an increase in trigeminal nerve terminal activity around large cerebral and meningeal arteries, leading to vasodilatation. Because prostaglandin E(2) (PGE(2)) is elevated in cephalic venous blood during migraine attacks, and is also capable of inducing headache in healthy volunteers, we hypothesize that PGE(2) dilatory receptors, EP(2) and EP(4), mediate the response.. By the use of specific agonists and antagonists, the dilatory effect of PGE(2) was characterized in rat cranial arteries by use of in vivo and in vitro methods. Furthermore, EP(2) and EP(4) quantitative messenger RNA (mRNA) receptor expression was studied in the rat craniovascular system.. Our results suggest that EP(4), and to a lesser degree EP(2), receptors mediate the dilatory effect of PGE(2) in the craniovascular system in rats. Thus, antagonism of these receptors might be of therapeutic relevance in migraine.

Topics: Adenine; Alprostadil; Animals; Cerebral Arteries; Dinoprostone; Enzyme Inhibitors; Male; Meningeal Arteries; Migraine Disorders; Prostaglandin Antagonists; Rats; Rats, Sprague-Dawley; Receptors, Prostaglandin E, EP2 Subtype; Receptors, Prostaglandin E, EP4 Subtype; RNA, Messenger; Trigeminal Nerve; Vasodilation; Xanthones