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 slight vasodilatory effect (max 10%). N-omega-nitro-L-arginine methyl ester and N-omega-Nitro-L-arginine in the range 10(-8)-10(-4) mol . l(-1) caused dose-dependent increases in coronary resistance. The vasodilatory action of L-arginine was abolished when the preparation was pretreated with 10(-4) mol . l(-1) N-omega-nitro-L-arginine or N-omega-nitro-L-arginine methyl ester. Nitroprusside alone at 1 mmol . l(-1) induced a maximum vasodilation (30%) of the coronary system. Methylene blue a known inhibitor of guanylate cyclase, induced a strong vasoconstriction (already significant at 10(-5) mol . l(-1)) and was able to overcome the vasodilative effect of nitroprusside. The endothelial nitric oxide agonists acetylcholine and serotonin, established in mammalian vessels, also mediate vasodilation in trout coronary system. In 50% of preparations, acetylcholine induced a biphasic response with vasodilation at low concentration (max 15% at 10(-8) mol . l(-1)). Serotonin displayed a dose-response vasodilation in the range 10(-8)-10(-4) mol . l(-1) (max 20%). These vasodilative effects were reduced or abolished by 10(-4) mol . l(-1) L-NA. These data support the existence of NO-mediated vasodilation mechanisms in the trout coronary system.