EVIDENCE FOR NO-DEPENDENT VASODILATION IN THE TROUT (ONCORHYNCHUS-MYKISS) CORONARY SYSTEM

The effects of L-arginine, and its analogues N-omega-nitro-L-arginine methyl ester and N-omega-nitro-L-arginine on vascular resistance were investigated in the intact coronary system of an isolated non-working trout heart preparation. L-Arginine, at 10(-8) mol . l(-1)induced a sl ight vasodilatory effect (max 10%). N-omega-nitro-L-arginine methyl es ter and N-omega-Nitro-L-arginine in the range 10(-8)-10(-4) mol . l(-1 ) caused dose-dependent increases in coronary resistance. The vasodila tory action of L-arginine was abolished when the preparation was pretr eated with 10(-4) mol . l(-1) N-omega-nitro-L-arginine or N-omega-nitr o-L-arginine methyl ester. Nitroprusside alone at 1 mmol . l(-1) induc ed a maximum vasodilation (30%) of the coronary system. Methylene blue a known inhibitor of guanylate cyclase, induced a strong vasoconstric tion (already significant at 10(-5) mol . l(-1)) and was able to overc ome the vasodilative effect of nitroprusside. The endothelial nitric o xide agonists acetylcholine and serotonin, established in mammalian ve ssels, also mediate vasodilation in trout coronary system. In 50% of p reparations, acetylcholine induced a biphasic response with vasodilati on at low concentration (max 15% at 10(-8) mol . l(-1)). Serotonin dis played a dose-response vasodilation in the range 10(-8)-10(-4) mol . l (-1) (max 20%). These vasodilative effects were reduced or abolished b y 10(-4) mol . l(-1) L-NA. These data support the existence of NO-medi ated vasodilation mechanisms in the trout coronary system.