Vasoactivity of Prostanoids In the Trout (oncorhynchus-mykiss) Coronary System - Modification By Noradrenaline

An isolated non-working trout heart, cannulated through the coronary artery and perfused with oxygenated saline with a coronary pressure head of 3.0 kPa has been used in this study. Effects on the coronary resistance of catecholamines, thromboxanes (TXs) and prostacyclin (PGI2) were analyzed. The effects of PGI2 and TXs in presence of noradrenaline were also evaluated. Both adrenaline and noradrenaline vasoconstrict the trout coronary system, noradrenaline being more potent than adrenaline. TXA2 induces 45% vasoconstriction at 10(-6)M, while TXB2 at the same concentration is a slight vasodilator. PGI2 acts as a weak vasodilator (about 20% decrease in resistance at 10(-6)M). In presence of 10(-7)M noradrenaline, 10(-8)M TXA2 reduces the vasoconstriction induced by the catecholamine alone from 60% to about 15%. Under similar conditions, 10(-9)M PGI2 potentiates the vasoconstrictive response induced by noradrenaline while a much higher PGI2 concentration (10(-6)M) completely abolishes the vasoconstriction. The beta-receptor antagonist propranolol induces vasoconstriction, and 10(-9)M PGI2 in presence of propranolol further increases the vasoconstriction. The alpha-receptor antagonist phentolamine induces vasodilation and 10(-9)M PGI2 does not affect coronary resistance induced by phentolamine. These results imply a possible interaction between noradrenaline and prostanoids (TXs and PGI2) in the vasomotion of trout coronary system.