Analysis of relaxin deficient mice

Abstract

The corpus luteum of pregnancy is the major source of circulating relaxin in mice and rats [1]. Both messenger RNA and peptide have also been detected in the uterus, brain and prostate gland [2–4]. Binding sites for relaxin include uterus, cervix, mammary gland, nipple, pubic symphysis, cardiac atrium and brain [5–8]. Much of our knowledge of the biological actions of relaxin has been derived from studies in the rat. Removal of the source of circulating relaxin by bilateral ovariectomy established that relaxin in combination with estrogen is required for normal parturition to occur [9]. Similar results were obtained by Sherwood and coworkers in a series of experiments using passive immunization with monoclonal antibodies specific for rat relaxin to neutralize endogenous activity [10]. Underdeveloped mammary glands and nipple with resultant poor lactation performance [11, 12] and effects on cervical softening [13], vaginal growth [14], and water consumption [15] were also observed.