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Celso E. Gomez-Sanchez, Channels and Pumps in Aldosterone-Producing Adenomas, The Journal of Clinical Endocrinology & Metabolism, Volume 99, Issue 4, 1 April 2014, Pages 1152–1156, https://doi.org/10.1210/jc.2014-1062
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Primary aldosteronism is the most common cause of secondary hypertension, with a prevalence of about 5% of the general hypertensive population and 10% of patients referred to hypertension specialty clinics. Aldosterone-producing adenomas (APAs) account for approximately 30–50% of cases of primary aldosteronism, and idiopathic hyperaldosteronism accounts for most of the rest of the cases. Aldosterone synthesis is regulated primarily by the renin-angiotensin system, potassium, ACTH, and to a lesser degree other peptides (1). Isolated adrenal zona glomerulosa and fasciculata cells from different species maintain a negative membrane resting potential determined by regulating membrane permeability to potassium (2, 3). Zona glomerulosa cells with hyperpolarized resting membrane voltages are steroidogenically inactive (4). Stimulation with angiotensin II, ACTH, or potassium results in membrane depolarization, opening of plasma membrane calcium channels, and mobilization of intracellular calcium, which increases activation of the calcium-calmodulin pathway, ultimately resulting in an increase in steroid biosynthesis and secretion (1). Several potassium channels have been described in rodent, bovine, and human adrenal cells, including inward rectifying and leak potassium currents that provide background potassium currents (reviewed in Ref. 3).
