Adrenal cell-differentiated functions and, therefore, their steroidoge
nic capacity can be regulated in an opposite direction by insulin-like
growth factor I (IGF-I) and transforming growth factor-beta(1) (TGF b
eta(1)). The enhanced steroidogenic responsiveness of bovine and ovine
adrenal cells treated with IGF-I can be explained by its positive eff
ects on the number of corticotropin (ACTH) and angiotensin II (A-II) r
eceptors associated with an increase in the alpha(s) and alpha(i) subu
nits of G proteins but also by its effects on several steps of the ste
roidogenic pathway. In contrast, TGF beta(1) is a potent inhibitor of
differentiated functions of both bovine and ovine adrenal cells. TGF b
eta(1) reduces ACTH and A-II receptor number, inhibits cAMP formation,
and decreases several steroidogenic enzyme activities. The physiologi
cal role of these peptides in adrenal cells is strengthened by the fac
t that both are synthetized and secreted by these cells and that their
secretion can be regulated by the specific hormones, ACTH and A-II.