Liberation of prostaglandin-like substances from the isolated coronary artery in presence of angiotensin and of 4-methylesculetin.
The aim of this work is to study the mechanism by which 4-Methylesculetin (4-ME) causes the relaxation or inhibits the Angiotensin II (ATN 2) induced contraction in the smooth muscle. The effect of 4-Me, alone or associated with Ascorbic Acid, on basal tone and ATN 2 induced contraction of isolated coronary strips have been studied. Experiments have been carried out in presence of Lysine Acetylsalicylate (LAS) and Indomethacin (IN), known inhibitors of prostaglandin-synthetase. Both LAS and IN decrease but not abolish, the 4-ME induced relaxation and suppressed the depressive effect of 4-ME on the ATN 2 dependent contraction. From R.I.A. tests results that 6-Keto PGF1 alpha (prostacyclines stable metabolite) concentration increased with the addition of 4-ME to the bath. 6-Keto PGF1 alpha concentration was drastically reduced after IN and LAS use. Therefore, it seems reasonable to conclude that 4-ME influence could be mediated by prostacyclines release in the smooth muscle.
D000804:Angiotensin II / Q000037:antagonists & inhibitors*; D000818:Animals; D001205:Ascorbic Acid / Q000494:pharmacology; D001241:Aspirin / Q000031:analogs & derivatives / Q000494:pharmacology; D002417:Cattle; D003331:Coronary Vessels / Q000187:drug effects* / Q000378:metabolism; D004347:Drug Interactions; D066298:In Vitro Techniques; D007213:Indomethacin / Q000494:pharmacology; D008239:Lysine / Q000031:analogs & derivatives / Q000494:pharmacology; D009131:Muscle, Smooth, Vascular / Q000187:drug effects*; D011453:Prostaglandins / Q000378:metabolism*; D012603:Scopoletin / Q000494:pharmacology*; D014468:Umbelliferones / Q000494:pharmacology*
D011453:Prostaglandins; D014468:Umbelliferones; D000804:Angiotensin II; D008239:Lysine; D012603:Scopoletin; D001205:Ascorbic Acid; D001241:Aspirin; C010395:acetylsalicylic acid lysinate; D007213:Indomethacin