Liberation of prostaglandin-like substances from the isolated coronary artery in presence of angiotensin and of 4-methylesculetin.

Abstract

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.