Regulation of Aldosterone Biosynthesis by Na+/H+Antiport: Relationships between Intracellular pH and Angiotensin II*

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Abstract
Recent studies on the regulation of aldosterone biosynthesis have revealed that inhibitors of sodium influx, e.g. amiloride, can inhibit adrenal steroidogenesis with a pharmacological profile suggestive of a Na+/H+ antiport system. We have examined the existence of a Na+/H+ antiport system and its regulation of Na influx and intracellular pH (pH;) in bovine adrenal zona glomerulosa cells. NH4Cl-induced 22Na uptake by zona glomerulosa cells was dose dependently inhibited by ethylisopropylamiloride (EIPA), amiloride, and benzamil with ED50 values of 0.02, 4.30, and 199 μM, respectively. Angiotensin II (All; 100 nM) caused an initial transient acidification, followed by prolonged alkalinization. The hormone equipotently increased pH; and stimulated aldosterone secretion, with ED50 values of 1.2 and 1.4 nM, respectively. All-induced alkalinization was suppressed by EIPA, amiloride, and benzamil, with ED50 values of 0.6, 79, and 440 /μM, respectively. This increase in pH; induced by All was dependent upon the extracellular sodium concentration (ED50 values = 2.8 mM) and was blunted in sodium-free medium. All-stimulated aldosterone synthesis was also inhibited by EIPA, amiloride, and benzamil, with ED50 values of 0.07, 34, and 330 /μM, respectively. The time course of activation by angiotensin II on aldosterone secretion was also dependent upon extracellular sodium concentration during a 2- h period. These results document that intracellular pH is regulated through the Na+/H+ exchange system and suggest that the pH change induced by All might be associated with its regulation of steroidogenesis in bovine adrenal zona glomerulosa cells. (Endocrinology124: 1925-1931, 1989)

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