[Nitric oxide in the physiopathology of myocardial dysfunction in heart failure]

Nitric oxide (NO) modulates several parameters of myocardial function at the autocrine and paracrine level. Various studies have demonstrated that endogenously NO, regulates myocardial contractility, distensibility, heart rate, coronary vasodilation, myocardial oxygen consumption, mitochondrial respiration and apoptosis. In pathological situations, particularly heart failure (HF), NO synthesis and activity are altered and its effects are controversial. Thus, NO can have beneficial or deleterious actions, depending on: (i) the cellular and enzymatic source, (ii) the amount produced and/or released, (iii) the presence of reactive oxygen species, (iv) interactions with neurohumoral and other stimuli, (v) the tanget issue and (vi) the activation of different cyclic GMP (cGMP)-dependent and independent subcellular signal transduction pathways. In this paper we review the main physiological actions of NO in normal myocardial function and its role in the pathophysiology of HF, as well as the cellular and molecular mechanisms underlying these effects. We also include a brief mention of therapeutic approaches are which directly or indirectly related with the bioavailability of this mediator.