Relaxin, initially identified as a hormone of pregnancy, is now known to exert different pleiotropic effects in both males and females. These pleotropic effects are physiological roles related to cardiovascular and renal systems such as antiinflammatory, antifibrotic, anti-hypertrophic, antiapoptotic. Relaxin has been reported to alter various gene expressions such as TGF-β (Transforming growth factor-β), MMP (matrix metalloproteinase) and
activate various signaling pathways such as cAMP (cyclic adenosine monophosphate), cGMP (cyclic guanosine monophosphate), MAPK (mitogen-activated protein kinase). Thus, relaxin is known to have an inhibitory role on cardiac fibrosis as well as protective effect on vascular functions. Relaxin shows these effects by binding to RXFP1 receptor (Relaxin/insulin-like family peptide receptor 1). RXFP1 is in the G protein coupled receptor family. Studies show that RXFP1 is present at different localizations (vascular smooth muscle cells or endothelial cells) in different vessel beds. In this review, the cellular mechanisms of relaxin effects on cardiovascular system and the effects of different vascular beds are presented together with animal models.

Relaxin Serelaxin Heart failure Fibrosis Vasodilatation