myocardial fibrosis is a common endpoint in a variety of cardiac pathologies. it results from excessive accumulation of collagen and other materials that together comprise the extracellular matrix (ecm). in the past decade, the peptide hormone relaxin has emerged as an important regulator of the ecm within several organs, including the heart, and has been suggested as a novel therapeutic agent for the treatment of fibrotic disorders. this review summarises research on the anti-fibrotic actions of relaxin, outlines the potential mechanisms by which relaxin regulates the ecm in cardiovascular tissues and examines the implications of this research for the management of heart disease. some of the contradictions in the literature are also addressed in order to clarify the role of relaxin as an anti-fibrotic factor in vivo.

Two experiments were performed to evaluate the influence of relaxin on the fertility of gilts inseminated with aged boar semen. For experiment 1, oestrus was induced in 43 Yorkshire × Landrace gilts by injection of 400 i.u. PMSG plus 200 i.u. hCG. At 24 h after oestrus detection, gilts were inseminated with fresh semen (1 to 2 day old; no. = 15), aged semen (5 to 6 days old; no. = 15) or aged semen containing 400 fig/l of relaxin added at the time of semen extension (no. = 13). Pregnancy rates 24 days after insemination were lower in gilts receiving aged semen (P < 0·05), an effect not prevented by added relaxin. There was no effect of either semen age or relaxin on numbers of embryos. In experiment 2, the ejaculates of eight boars were extended with or without the addition of 400 fig/I relaxin and motility monitored for 7 days. Fresh sperm motility decreased from 87-5 (s.e. 2·5)% at collection to 71-2 (s.e. 3·3)% after 7 days. The attenuation of sperm motility was not affected by relaxin.