{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T00:52:41Z","timestamp":1790815961370,"version":"4.1.0"},"reference-count":73,"publisher":"The Endocrine Society","issue":"12","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2015,12,1]]},"abstract":"<jats:p>Aldosterone-producing adenoma (APA) is a major cause of primary aldosteronism, leading to secondary hypertension. Somatic mutations in the gene for the \u03b11 subunit of the Na+\/K+-ATPase were found in about 6% of APAs. APA-related \u03b11 subunit of the Na+\/K+-ATPase mutations lead to a loss of the pump function of the Na+\/K+-ATPase, which is believed to result in membrane depolarization and Ca2+-dependent stimulation of aldosterone synthesis in adrenal cells. In addition, H+ and Na+ leak currents via the mutant Na+\/K+-ATPase were suggested to contribute to the phenotype. The aim of this study was to investigate the cellular pathophysiology of adenoma-associated Na+\/K+-ATPase mutants (L104R, V332G, G99R) in adrenocortical NCI-H295R cells. The expression of these Na+\/K+-ATPase mutants depolarized adrenal cells and stimulated aldosterone secretion. However, an increase of basal cytosolic Ca2+ levels in Na+\/K+-ATPase mutant cells was not detectable, and stimulation with high extracellular K+ hardly increased Ca2+ levels in cells expressing L104R and V332G mutant Na+\/K+-ATPase. Cytosolic pH measurements revealed an acidification of L104R and V332G mutant cells, despite an increased activity of the Na+\/H+ exchanger. The possible contribution of cellular acidification to the hypersecretion of aldosterone was supported by the observation that aldosterone secretion of normal adrenocortical cells was stimulated by acetate-induced acidification. Taken together, mutations of the Na+\/K+-ATPase depolarize adrenocortical cells, disturb the K+ sensitivity, and lower intracellular pH but, surprisingly, do not induce an overt increase of intracellular Ca2+. Probably, the autonomous aldosterone secretion is caused by the concerted action of several pathological signaling pathways and incomplete cellular compensation.<\/jats:p>","DOI":"10.1210\/en.2015-1466","type":"journal-article","created":{"date-parts":[[2015,9,29]],"date-time":"2015-09-29T17:00:31Z","timestamp":1443546031000},"page":"4582-4591","source":"Crossref","is-referenced-by-count":63,"title":["Pathogenesis of Adrenal Aldosterone-Producing Adenomas Carrying Mutations of the Na+\/K+-ATPase"],"prefix":"10.1210","volume":"156","author":[{"given":"J.","family":"Stindl","sequence":"first","affiliation":[{"name":"Medical Cell Biology, University of Regensburg, 93053 Regensburg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P.","family":"Tauber","sequence":"first","affiliation":[{"name":"Medical Cell Biology, University of Regensburg, 93053 Regensburg, 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