Acute neurohumoral modulation of diastolic function

Diastole plays a central role in cardiovascular homeostasis. Its two main determinants, myocardial relaxation and passive properties of the ventricular wall, are nowadays regarded as physiological mechanisms susceptible of active modulation. Furthermore, diastolic dysfunction and heart failure with normal ejection fraction (previously called diastolic heart failure) are two subjects of major clinical relevance and an intense area of research. The role of several neurohumoral mediators like angiotensin-II and endothelin-1 on the modulation of diastolic function was systematically described as having only chronic deleterious effects such as cardiac hypertrophy and fibrosis. However, over the last years a growing body of evidence described a new role for several peptides on the acute modulation of diastolic function. In the acute setting, some of these mediators may have the potential to induce an adaptive cardiac response. In this review, we describe the role of angiotensin-II, endothelin-1, nitric oxide, urotensin-II and ghrelin on the acute modulation of diastolic function, emphasizing its pathophysiological relevance. Only a thorough understanding of diastolic physiology as well as its active modulation, both in the acute and chronic settings, will improve our knowledge on diastolic dysfunction and allow us to solve the enigmas of heart failure with normal ejection fraction.