{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,29]],"date-time":"2026-01-29T23:31:47Z","timestamp":1769729507021,"version":"3.49.0"},"reference-count":54,"publisher":"The Endocrine Society","issue":"12","license":[{"start":{"date-parts":[[2025,10,14]],"date-time":"2025-10-14T00:00:00Z","timestamp":1760400000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000062","name":"National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["2R01DK123694"],"award-info":[{"award-number":["2R01DK123694"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["R01HL138241"],"award-info":[{"award-number":["R01HL138241"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2025,11,6]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Primary aldosteronism (PA) is characterized by autonomous aldosterone (Aldo) production, resulting in blood volume\/electrolyte imbalance and hypertension. Intracellular calcium (Ca2+) is the principal signal driving Aldo synthesis in adrenal zona glomerulosa (zG) cells, and mutations in ion transport genes that regulate Ca2+ are frequently mediators of PA. When organized in intact rosette structures, zG cells are voltage oscillators; stimulation by angiotensin II (AngII) or loss of TWIK-related acid-sensitive potassium (TASK) channel function evokes stereotypic Ca2+ oscillations with bursting activity proportional to increased steroidogenesis. Here, we delineate the role of the osmolar-volume regulatory axis in the control of Ca2+ and Aldo production in adrenal slices. Strikingly, in both pharmacological and genetic models of PA, extracellular osmolarity (OSMEC) potently and reversibly regulated Aldo secretion and Ca2+ signaling. Elevated OSMEC progressively suppressed Aldo production from AngII-stimulated adrenal slices and strongly inhibited autonomous production in both zG-specific TASK knockout slices and wild-type slices incubated with TASK inhibitors (TIs). To determine if the effects of OSMEC on Ca2+ dynamics were causative, we imaged adrenal slices expressing zG-specific GCaMP6f incubated in variable osmotic media with TIs or AngII. Consistent with Aldo suppression, increasing osmolarity proportionally reduced the number of active cells and the Ca2+ activity of bursting cells evoked by TASK loss of function or AngII stimulation. Collectively, our findings identify OSMEC as a broad regulator of zG excitability and adrenal steroidogenesis, and suggest that targeting volume-regulatory mechanisms such as the Na+-K+-2Cl\u2212 cotransporter may offer a novel strategy to suppress Aldo autonomy in PA.<\/jats:p>","DOI":"10.1210\/endocr\/bqaf147","type":"journal-article","created":{"date-parts":[[2025,10,14]],"date-time":"2025-10-14T11:46:37Z","timestamp":1760442397000},"source":"Crossref","is-referenced-by-count":2,"title":["Osmolarity Controls Oscillatory Calcium Signaling to Reduce Autonomous Aldosterone Production in Zona Glomerulosa Cells"],"prefix":"10.1210","volume":"166","author":[{"given":"Mohamed","family":"Diagne","sequence":"first","affiliation":[{"name":"Department of Stem Cell and Regenerative Biology, Harvard University , Cambridge, MA 02138 ,","place":["USA"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Molly R","family":"Gerding","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, University of Virginia , Charlottesville, VA 22908-0735 ,","place":["USA"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"David T","family":"Breault","sequence":"additional","affiliation":[{"name":"Division of Endocrinology, Boston Children\u2019s Hospital , Boston, MA 02115 ,","place":["USA"]},{"name":"Department of Pediatrics, Harvard Medical School , Boston, MA 02115 ,","place":["USA"]},{"name":"Broad Institute of MIT and Harvard , Cambridge, MA 02142 ,","place":["USA"]},{"name":"Harvard Stem Cell Institute , Cambridge, MA 02138 ,","place":["USA"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Edward H","family":"Nieh","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, University of Virginia , Charlottesville, VA 22908-0735 ,","place":["USA"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mark P","family":"Beenhakker","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, University of Virginia , Charlottesville, VA 22908-0735 ,","place":["USA"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Paula Q","family":"Barrett","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, University of Virginia , Charlottesville, VA 22908-0735 ,","place":["USA"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2539-1346","authenticated-orcid":false,"given":"Nick A","family":"Guagliardo","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, University of Virginia , Charlottesville, VA 22908-0735 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