Abstract

Cardiovascular (CV) diseases are caused by vascular dysfunction. The enhanced sensitivity to vasoconstrictors, reduced endothelium-derived vasodilators nitric oxide (NO) and prostacyclin (PGI2), and endothelium-derived hyperpolarization (EDH) indicate CV dysfunction. In recent years, recombinant human relaxin, known as serelaxin, has emerged as a new vasoactive drug that is useful in acute heart failure. First part of this review article encompasses the role of endogenous relaxin in CV homeostasis. Subsequently, vascular effects of serelaxin and the underlying modes of action in comparison to other vasodilators are discussed. Finally, the usefulness of treatment with serelaxin in vascular dysfunction in different CV diseases, particularly due to oxidative stress, is explained.

Keywords: Recombinant human relaxin, acute heart failure, cardiovascular, endothelium-derived hyperpolarization, homeostasis, nitric oxide, prostacyclin, vasoconstrictors.

Graphical Abstract