Can stress make you relax?

This editorial refers to ‘Stretch-induced compliance: a novel adaptive biological mechanism following acute cardiac load’ by A.M. Leite-Moreira et al., pp. 656–667. Cardiac force adaptations to increased preload are well-known, with a biphasic increase in contractility, i.e. a rapid phase that involves enhanced calcium sensitivity of cardiac myofilaments (the basis of the Frank–Starling mechanism)1 and a delayed phase due to an increased Calcium transient (the basis of the classical Anrep effect).2 Concurrent adaptations of ventricular compliance and diastolic pressure are much less defined. Increased compliance with ensuing fibre and sarcomere stretch (within physiological range of sarcomere length) would allow further recruitment of diastolic reserve to optimize ventricular filling and the adaptation of contractility (according to the earlier mechanisms) in the face of increased venous return (e.g. during exercise). Such phenomena have been proposed in response to paracrine release of myocardial ‘relaxants’ such as natriuretic peptides (NPs) and nitric oxide (NO).3 In this issue of Cardiovascular Research4, Leite-Moreira (father and son) and colleagues now systematically examine the occurrence of stretch-induced compliance adaptation in several animal and human experimental preparations and propose an underlying mechanism. [...