Although the major source of relaxin in pigs is the corpus luteum of p
regnancy, there is now evidence for relaxin gene expression and transl
ation into protein in the theca interna cells of the preovulatory foll
icle, the corpus luteum of the cycle and the uterus. The theca interna
cells retain their ability to express the relaxin gene and protein fo
llowing ovulation. During the early stages of development of the corpu
s luteum, the theca-derived small lutein cells are the source of the r
elaxin transcript. As the corpus luteum becomes fully functional, ther
e is a switch in the site of relaxin synthesis h om small theca-derive
d lutein cells to large granulosa-derived cells. In the absence of lut
eolysis, this switch is accompanied by a dramatic rise in relaxin synt
hesis. Relaxin has been identified in boar seminal plasma and can main
tain or increase sperm motility. However, a source of relaxin in the b
oar has not been identified. Relaxin is an important regulator of uter
ine function during pregnancy acting systemically to suppress myometri
al activity and promote cervical dilation at parturition. The changes
in thecal relaxin production during follicle development and its abili
ty to promote growth and changes in proteolytic enzyme activity of gra
nulosa cells in vitro have led to the concept of: an autocrine or para
crine role for relaxin within the follicle. Uterotrophic effects of re
laxin have been reported in rodents and swine and support the hypothes
is that relaxin promotes uterine growth and expansion in early pregnan
cy to accommodate the growing fetuses. Mammotrophic effects of relaxin
in rodents have now been extended to pigs, with evidence that relaxin
is necessary for normal mammary parenchymal development in late pregn
ancy. In most instances the mechanisms responsible for, and the physio
logical significance of, these diverse biological effects remain to be
elucidated.