{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,13]],"date-time":"2026-06-13T18:16:09Z","timestamp":1781374569426,"version":"3.54.1"},"reference-count":77,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Cell Physiology"],"published-print":{"date-parts":[[2011,11]]},"abstract":"<jats:p>Urinary acidification in the collecting duct is mediated by the activity of H<jats:sup>+<\/jats:sup>-ATPases and is stimulated by various factors including angiotensin II and aldosterone. Classically, aldosterone effects are mediated via the mineralocorticoid receptor. Recently, we demonstrated a nongenomic stimulatory effect of aldosterone on H<jats:sup>+<\/jats:sup>-ATPase activity in acid-secretory intercalated cells of isolated mouse outer medullary collecting ducts (OMCD). Here we investigated the intracellular signaling cascade mediating this stimulatory effect. Aldosterone stimulated H<jats:sup>+<\/jats:sup>-ATPase activity in isolated mouse and human OMCDs. This effect was blocked by suramin, a general G protein inhibitor, and GP-2A, a specific G<jats:sub>\u03b1q<\/jats:sub>inhibitor, whereas pertussis toxin was without effect. Inhibition of phospholipase C with U-73122, chelation of intracellular Ca<jats:sup>2+<\/jats:sup>with BAPTA, and blockade of protein kinase C prevented the stimulation of H<jats:sup>+<\/jats:sup>-ATPases. Stimulation of PKC by DOG mimicked the effect of aldosterone on H<jats:sup>+<\/jats:sup>-ATPase activity. Similarly, aldosterone and DOG induced a rapid translocation of H<jats:sup>+<\/jats:sup>-ATPases to the luminal side of OMCD cells in vivo. In addition, PD098059, an inhibitor of ERK1\/2 activation, blocked the aldosterone and DOG effects. Inhibition of PKA with H89 or KT2750 prevented and incubation with 8-bromoadenosine-cAMP mildly increased H<jats:sup>+<\/jats:sup>-ATPase activity. Thus, the nongenomic modulation of H<jats:sup>+<\/jats:sup>-ATPase activity in OMCD-intercalated cells by aldosterone involves several intracellular pathways and may be mediated by a G<jats:sub>\u03b1q<\/jats:sub>protein-coupled receptor and PKC. PKA and cAMP appear to have a modulatory effect. The rapid nongenomic action of aldosterone may participate in the regulation of H<jats:sup>+<\/jats:sup>-ATPase activity and contribute to final urinary acidification.<\/jats:p>","DOI":"10.1152\/ajpcell.00076.2011","type":"journal-article","created":{"date-parts":[[2011,8,11]],"date-time":"2011-08-11T04:57:24Z","timestamp":1313038644000},"page":"C1251-C1261","source":"Crossref","is-referenced-by-count":51,"title":["Aldosterone stimulates vacuolar H<sup>+<\/sup>-ATPase activity in renal acid-secretory intercalated cells mainly via a protein kinase C-dependent pathway"],"prefix":"10.1152","volume":"301","author":[{"given":"Christian","family":"Winter","sequence":"first","affiliation":[{"name":"Institute of Physiology, Center for Integrative Human Physiology, University of Zurich, Zurich, Switzerland;"},{"name":"Clinics of Urology, University Hospital D\u00fcsseldorf, D\u00fcsseldorf, Germany;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicole 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