SYMPATHOADRENAL REGULATION OF ADRENOCORTICAL STEROIDOGENESIS

Sympathoadrenal regulation of adrenocortical steroidogenesis was studi ed on a physiological, cellular, molecular and morphological level. Th e effects of nerve activation and of epinephrine (EPI) on adrenal cort icosteroid release were compared in isolated perfused pig adrenals wit h preserved nerve supply. Splanchnic nerve activation as well as perfu sion with EPI provoked a siginificant release of cortisol, aldosterone and androstenedione. In cultured bovine adrenocortical cells steroid secretion and accumulation of P450(scc), P450(17 alpha), P450(c21) and P450(11 beta) mRNAs were studied after stimulation with EPI with or w ithout propranolol or phentolamine. Incubation with EPI stimulated ste roidogenesis and increased the levels of all four P450-mRNAs. The beta -adrenergic antagonist propranolol totally blocked the effects of EPI while the alpha-antagonist phentolamine had no effect. Using immunohis tochemistry, adrenals were studied morphologically. The contact zones of the two cell types were investigated on an electron microscopical l evel. Cortical and medullary cells were closely interwoven with cortic al and chromaffin cells in direct apposition, providing the possibilit y for paracrine interactions. It is concluded that the release of cort icosteroids can be stimulated through the sympatho-adrenal system. The stimulatory action of EPI upon adrenal steroid formation and accumula tion of all four P450-mRNAs requires beta-adrenergic receptors. Taking into consideration the close colocalization of cortical and medullary tissue, this stimulation may be mediated by chromaffin cells in a par acrine manner.