The search for gonadal proteins that regulate pituitary FSH led to the isol
ation of inhibins and activins. As members of the transforming growth facto
r beta (TGF beta) superfamily of growth and differentiation factors, these
proteins have been shown subsequently to affect a range of tissues and syst
ems beyond their role in reproduction. Studies on the expression and synthe
sis of activins in the male reproductive tract have localized these protein
s in the testis, epididymis and prostate. In general, activins regulate cel
l proliferation and, consequently, the expression and localization of activ
in subunit mRNAs and proteins within these organs must be discrete. Activin
ligand bioactivity is dependent on the presence of the appropriate recepto
rs and signalling systems, but activin Ligand formation or access to recept
ors is regulated by the formation of inhibins or by activin-binding protein
s such as follistatin. This review examines the evidence that the capacity
to synthesize activins and to regulate activin bioactivity resides in the c
ells of the male reproductive tract. It is concluded that activins exert th
eir effects through local (autocrine or paracrine) mechanisms, rather than
through endocrine systems. The interplay between the inhibins or follistati
ns provides a degree of regulation of activin bioactivity before ligand sig
nalling events. The challenge for the future is to determine whether there
is any difference between the action of individual activin ligands or wheth
er these proteins are functionally redundant, indicating that compensatory
mechanisms are essential for male reproductive tract function.