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.