Effect of ACTH on prostaglandin induced vascular permeability.
Increased vascular permeability was induced by prostaglandin E2 (PGE1), arachidonic acid and compound 48/80 in male rats. Natural ACTH in a dose-dependent manner inhibited Evans blue exudation elicited by arachidonic acid or compound 48/80, however, it was ineffective against PGE1. ACTH4--10 (d-Phe7 and 1-Phe7) injected together with the prophlogistic agents depressed the arachidonic acid and compound 48/80 induced vascular reaction. Indomethacin pretreatment inhibited the effect of arachidonic acid on vascular permeability suggesting that arachidonic acid evoked its vascular activity by means of affecting the endogenous synthesis of prostaglandins and, on the other hand, the prostaglandin system played a role in the vascular permeability inducing effect of compound 48/80. ACTH4--10 peptide fragments free of steroidogenic action and natural ACTH inhibited locally the in vivo formation of PGS from arachidonic acid in the rat skin, resulting in a nonspecific decrease of local inflammation.
D000324:Adrenocorticotropic Hormone / Q000494:pharmacology*; D000818:Animals; D001095:Arachidonic Acids / Q000037:antagonists & inhibitors; D002199:Capillary Permeability / Q000187:drug effects*; D004305:Dose-Response Relationship, Drug; D008297:Male; D011458:Prostaglandins E / Q000037:antagonists & inhibitors* / Q000494:pharmacology; D051381:Rats; D012867:Skin / Q000098:blood supply; D003189:p-Methoxy-N-methylphenethylamine / Q000037:antagonists & inhibitors
D001095:Arachidonic Acids; D011458:Prostaglandins E; D003189:p-Methoxy-N-methylphenethylamine; D000324:Adrenocorticotropic Hormone