Nitric Oxide modulation of mechanical performance in the teleost heart

In mammals, nitric oxide (NO), produced by nitric oxide synthase (NOS) and released by myocardiocytes and/or endocardial and vascular endothelial cells, plays an important role in modulating both intrinsic and extrinsic cardiac regulatory mechanisms. Fish hearts show common structural and functional aspects with higher vertebrates and, at the same time, differences in cardiac ultrastructure, myoarchitecture (trabecular vs compact type), blood supply (lacunary vs vascular) and pumping performance (sensitivity to filling pressure). They may thus represent useful experimental models to study an early cardiac autocrine-paracrine function of NO, possibly revealing aspects of unity and diversity in heart design. This synopsis focuses on the role of NO in modulating mechanical performance in teleost hearts. We show that NO, through a cGMP-mediated mechanism, regulates basal cardiac performance and influences the preload-induced increases in cardiac output at a constant afterload and heart rate (i.e. Frank-Starling relationship), an intrinsic mechanism crucial for cardiac physiology in fish. Moreover, NO is involved in modulating cardiac response to important chemical stimuli such as exogenous Acetylcholine and Angiotensin II. The involvement of cardiac NOS system in fish is also stressed by the role played by NO in the determinism of cardiac dysfunction associated with a viral disease as shown in salmon. Finally, the use of an avascular teleost heart, as conceptual tool, illustrates the importance of a paracrine role of endocardial endothelium NO during the evolution of cardiovascular system in lower vertebrates.