Recent Advances: The Fasciculata and Glomerulosa as Two Distinct Glands

Abstract

In proposing that the adrenal zona fasciculata and zona glomerulosa function as two distinct glands under different regulatory control, New and Seaman (1970) suggested that an 11 β-hydroxylase defect might occur only in the fasciculata, sparing the glomerulosa from an 11 β-hydroxylase deficiency. The hypothesis accounts for the rise in aldosterone secretion observed in a patient with 11 β-hydroxylase deficiency after excessive DOC levels were suppressed during treatment. According to the proposal, the fasciculata suffers from an 11 β-hydroxylase defect and produces excessive DOC. Elevated circulating levels of DOC cause excessive renal tubular reabsorption of sodium, which suppresses renal renin production. The glomerulosa is deprived of the stimulation of the renin-angiotensin system required for aldosterone synthesis and low aldosterone secretion results (Fig. 8). When DOC secretion is suppressed by treatment, natriuresis occurs and renin-angiotensin levels consequently rise, stimulating the glomerulosa to synthesize aldosterone (Fig. 9). Because the glomerulosa, unlike the fasciculata, is spared the 11 β-hydroxylase defect, it can respond to this stimulation with an appropriate increase in aldosterone secretion, and serum and urinary aldosterone levels rise. The adrenal steroid biosynthetic pathways in this disorder according to this hypothesis are schematically depicted in Fig. 10.