when does relaxin start being produced during pregnancy
Relaxin In females, relaxin is produced mainly by the corpus luteum, in both pregnant [1] and nonpregnant[1] females; it rises to a peak within approximately 14 days of ovulation, and then declines in the absence of pregnancy, resulting in menstruation[citation needed]). During the first trimester of pregnancy, levels rise and additional relaxin is produced by the decidua. Relaxin's peak is reached during the 14 weeks of the first trimester and at delivery. It is known to mediate the hemodynamic changes that occur during pregnancy, such as increased cardiac output, increased renal blood flow, and increased arterial compliance. It also relaxes other pelvic ligaments.[6] It is believed to soften the pubic symphysis.
Breast development Progesterone, in conjunction with GH/IGF-1 similarly to estrogen, affects the development of the breasts during puberty and thereafter as well.[15][16][20] To a lesser extent than estrogen, progesterone contributes to ductal development at this time, as evidenced by the findings that progesterone receptor (PR) knockout mice or mice treated with the PR antagonist mifepristone show delayed (albeit eventually normal, due to estrogen acting on its own) ductal growth during puberty and by the fact that progesterone has been found to induce ductal growth on its own in the mouse mammary gland mainly via the induction of the expression of amphiregulin, the same growth factor that estrogen primarily induces to mediate its actions on ductal development.[22] In addition, progesterone produces modest lobuloalveolar development (alveolar bud formation or ductal sidebranching) starting at puberty,[15][20] specifically through activation of PRB (and notably not PRA),[23] with growth and regression of the alveoli occurring to some degree with each menstrual cycle.[15][16] However, only rudimentary alveoli develop in response to pre-pregnancy levels of progesterone and estrogen, and lobuloalveolar development will remain at this stage until pregnancy occurs, if it does.[16] In addition to GH/IGF-1, estrogen is required for progesterone to affect the breasts,[15][20] as estrogen primes the breasts by inducing the expression of the progesterone receptor (PR) in breast epithelial tissue.[23] In contrast to the case of the PR, ER expression in the breast is stable and differs relatively little in the contexts of reproductive status, stage of the menstrual cycle, or exogenous hormonal therapy.[23]