Incorporation of arachidonic acid and its release from rat Leydig cells

These results, that there is a different temporal profile of release of LH and G H by PDBu, a differential action of two PKC inhibitors on this release and also that an L-type CaZ+channel blocker can completely inhibit PDBu-induced release of GH but not LH, indicate strongly that regulation of hormone secretion by PKC is very differently organized in the cell types involved. It is known that LHRH-induced LH release is partly through Ca2+-channels that can be blocked by dihydropyridines (Mitchell & Johnson, 1987; Chang et al., 1986). However, the release of LH by PDBu is obviously not through this route. In somatotrophes though, the activation of PKC would appear to cause G H secretion solely through these channels. Interestingly, a marked secretagogue action of Ba2+ is apparent on the release of GH but not LH (Mitchell & Anderson, 1985) consistent with voltage-activation of Ca2+-channels occurring in the basal state of somatotrophes. Depolarization-induced 45Ca2 + influx through L-type Ca2+-channels is also known to be enhanced by PKC (Fink et al., 1987) and this may be the mechanism underlying phorbol-induced G H secretion. The differential action of the two PKC inhibitors on PDBu-induced G H and LH secretion suggests that the PKC activated in gonadotrophes compared with somatotrophes may be either a different isoform or differently compartmentalized. There are presently seven subspecies of PKC identified (Nishizuka, 1988) which appear to be distinctly localized between tissues. In addition, these isoforms can be differentially activated, consequently it would not be unreasonable to assume that the present results reflect differential inhibition of PKC subtypes with H7 and staurosporine. In conclusion then, our data are consistent with either different isoforms, or modes of action, of PKC being involved in phorbol ester action on gonadotrophes and somatotrophes.