{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T17:52:37Z","timestamp":1773424357687,"version":"3.50.1"},"reference-count":39,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2011,3]]},"abstract":"<jats:p>The genomic and nongenomic effects of aldosterone on the intracellular pH recovery rate (pHirr) via H<jats:sup>+<\/jats:sup>-ATPase and on cytosolic free calcium concentration ([Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>) were investigated in isolated proximal S3 segments of rats during superfusion with an Na<jats:sup>+<\/jats:sup>-free solution, by using the fluorescent probes BCECF-AM and FLUO-4-AM, respectively. The pHirr, after cellular acidification with a NH<jats:sub>4<\/jats:sub>Cl pulse, was 0.064 \u00b1 0.003 pH units\/min ( n = 17\/74) and was abolished with concanamycin. Aldosterone (10<jats:sup>\u221212<\/jats:sup>, 10<jats:sup>\u221210<\/jats:sup>, 10<jats:sup>\u22128<\/jats:sup>, or 10<jats:sup>\u22126<\/jats:sup>M with 1-h or 15- or 2-min preincubation) increased the pHirr. The baseline [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>was 103 \u00b1 2 nM ( n = 58). After 1 min of aldosterone preincubation, there was a transient and dose-dependent increase in [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>and after 6-min preincubation there was a new increase in [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>that persisted after 1 h. Spironolactone [mineralocorticoid (MR) antagonist], actinomycin D, or cycloheximide did not affect the effects of aldosterone (15- or 2-min preincubation) on pHirr and on [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>but inhibited the effects of aldosterone (1-h preincubation) on these parameters. RU 486 [glucocorticoid (GR) antagonist] and dimethyl-BAPTA (Ca<jats:sup>2+<\/jats:sup>chelator) prevented the effect of aldosterone on both parameters. The data indicate a genomic (1 h, via MR) and a nongenomic action (15 or 2 min, probably via GR) on the H<jats:sup>+<\/jats:sup>-ATPase and on [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>. The results are compatible with stimulation of the H<jats:sup>+<\/jats:sup>-ATPase by increases in [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>(at 10<jats:sup>\u221212<\/jats:sup>-10<jats:sup>\u22126<\/jats:sup>M aldosterone) and inhibition of the H<jats:sup>+<\/jats:sup>-ATPase by decreases in [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>(at 10<jats:sup>\u221212<\/jats:sup>or 10<jats:sup>\u22126<\/jats:sup>M aldosterone plus RU 486).<\/jats:p>","DOI":"10.1152\/ajprenal.00172.2010","type":"journal-article","created":{"date-parts":[[2010,12,30]],"date-time":"2010-12-30T01:23:55Z","timestamp":1293672235000},"page":"F682-F691","source":"Crossref","is-referenced-by-count":15,"title":["Genomic and nongenomic stimulatory effect of aldosterone on H<sup>+<\/sup>-ATPase in proximal S3 segments"],"prefix":"10.1152","volume":"300","author":[{"given":"D. C. 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