{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,8]],"date-time":"2026-05-08T21:34:00Z","timestamp":1778276040456,"version":"3.51.4"},"reference-count":43,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2008,11]]},"abstract":"<jats:p>The effects of aldosterone on the intracellular pH recovery rate (pHirr) via Na<jats:sup>+<\/jats:sup>\/H<jats:sup>+<\/jats:sup>exchanger and on the [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>were investigated in isolated rat S3 segment. Aldosterone [10<jats:sup>\u221212<\/jats:sup>, 10<jats:sup>\u221210<\/jats:sup>, or 10<jats:sup>\u22128<\/jats:sup>M with 1-h, 15- or 2-min preincubation (pi)] caused a dose-dependent increase in the pHirr, but aldosterone (10<jats:sup>\u22126<\/jats:sup>M with 1-h, 15- or 2-min pi) decreased it (these effects were prevented by HOE694 but not by S3226). After 1 min of aldosterone pi, there was a transient and dose-dependent increase of the [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>and after 6-min pi there was a new increase of [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>that persisted after 1 h. Spironolactone, actinomycin D, or cycloheximide did not affect the effects of aldosterone (15- or 2-min pi) but inhibited the effects of aldosterone (1-h pi) on pHirr and on [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>. RU 486 prevented the stimulatory effect of aldosterone (10<jats:sup>\u221212<\/jats:sup>M, 15- or 2-min pi) on both parameters and maintained the inhibitory effect of aldosterone (10<jats:sup>\u22126<\/jats:sup>M, 15- or 2-min pi) on the pHirr but reversed its stimulatory effect on the [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>to an inhibitory effect. The data indicate a genomic (1 h, via MR) and a nongenomic action (15 or 2 min, probably via GR) on [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>and on the basolateral NHE1 and are compatible with stimulation of the NHE1 by increases in [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>in the lower range (at 10<jats:sup>\u221212<\/jats:sup>M aldosterone) and inhibition by increases at high levels (at 10<jats:sup>\u22126<\/jats:sup>M aldosterone) or decreases in [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>(at 10<jats:sup>\u22126<\/jats:sup>M aldosterone plus RU 486).<\/jats:p>","DOI":"10.1152\/ajprenal.00048.2008","type":"journal-article","created":{"date-parts":[[2008,8,21]],"date-time":"2008-08-21T00:24:12Z","timestamp":1219278252000},"page":"F1342-F1352","source":"Crossref","is-referenced-by-count":21,"title":["Genomic and nongenomic dose-dependent biphasic effect of aldosterone on Na<sup>+<\/sup>\/H<sup>+<\/sup>exchanger in proximal S3 segment: role of cytosolic calcium"],"prefix":"10.1152","volume":"295","author":[{"given":"D. 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