Effects of ACTH and Angiotensin II on the Novel Cell Layer Without Corticosteroid-Synthesizing Activity in Rat Adrenal Cortex

Abstract

We previously reported the presence of a novel cell layer containing neither cytochrome P-45011β nor cytochrome P-450aldo in the rat adrenal cortex. As these cytochrome P-450s are terminal enzymes in biosynthetic pathways for gluco- and mineralocorticoids such as corticosterone and aldosterone, the cell layer can be regarded as inert in producing corticosteroids. This study was designed to examine the chronic effects of adrenocorticotropin (ACTH) or angiotensin II on the novel layer employing histochemical techniques. The novel layer in a normal rat was present between the zona glomerulosa (zG) and the zona fasciculata (zF) as a four- to six-cell stratum, where replicating cells positive to anti-bromodeoxyuridine (anti-BrdU) and anti-proliferating cell nuclear antigen (anti-PCNA) were abundant. When the plasma ACTH level was raised for 20 days, zF formed a thicker zone, while the width of the novel layer attenuated to one to two cells thick. Under this condition, replicating cells were concentrated around the interface of the increased zF and the attenuated layer. A high level of plasma angiotensin II concentration for 20 days caused proliferation of zG together with a decrease of the novel layer to two to three cells thick. In this case, replicating cells were found around the interface of zG and the novel layer. These results thus support our previous hypothesis that the novel layer without steroidogenic activity is a stem- or progenitor-cell zone of the adrenal cortex.