Role of nitric oxide in the control of coronary resistance in teleosts.

In mammals, the in vivo coronary blood flow and myocardial oxygen consumption are closely related via changes in coronary resistance in response to the metabolic demands of the myocardium. A fine neurohumoral regulation of coronary resistance holds true also in fish, and particularly in teleosts, where several vasoconstrictive and vasodilative mechanisms have been described, with numerous putative effectors, including prostanoids, acetylcholine, adrenaline, serotonin, adenosine, steroid hormones. Here, a resume is reported of the available evidence on the involvement of nitric oxide (NO) in the control of coronary resistance in teleosts and particularly in salmonids. Most of the evidence reported is from a comprehensive study performed on a Langedorff-type preparation of the isolated trout heart. Using a physio-pharmacological approach, the experiments performed on this preparation have demonstrated that trout coronary resistance is reduced by l-arginine (NOS substrate), nitroprusside and SNAP (NO donors) and is increased by the NOS inhibitors l-NNA and l-NAME. The vasodilation induced by nitroprusside is blocked by the guanylate cyclase inhibitor methylene blue. l-arginine increases NO release in the perfusate, while l-NNA reduces the release. NO release is inversely related with the coronary resistance. l-NNA inhibits the vasodilatory effects of acetylcholine, serotonin and adenosine. The vasodilation induced by adenosine is accompanied by NO release and involves stretch receptors. Hypoxia induces vasodilation and both adenosine and NO release in the preparation; the NO release under hypoxia is blocked by theophylline. On the whole these data indicate that NO plays a central role in the control of coronary resistance in trout. In particular, a main role for NO as an amplifier of the adenosine-mediated vasodilation under hypoxia can be hypothesized.