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This Article Full Text Full Text (PDF) All Versions of this Article: 296/5/F1185    most recent 90217.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Pergher, P. S. Articles by de Mello-Aires, M. Search for Related Content PubMed PubMed Citation Articles by Pergher, P. S. Articles by de Mello-Aires, M.

Direct action of aldosterone on bicarbonate reabsorption in in vivo cortical proximal tubule

Department of Physiology and Biophysics, Biomedical Sciences Institute, University of São Paulo, São Paulo, Brazil

Submitted 27 March 2008 ; accepted in final form 14 February 2009

The direct action of aldosterone (10^–12 M) on net bicarbonate reabsorption (J_HCO3^–) was evaluated by stationary microperfusion of an in vivo middle proximal tubule (S2) of rat kidney, using H ion-sensitive microelectrodes. Aldosterone in luminally perfused tubules caused a significant increase in J_HCO3^– from a mean control value of 2.84 ± 0.08 [49/19 (n° of measurements/n° of tubules)] to 4.20 ± 0.15 nmol·cm^–2·s^–1 (58/10). Aldosterone perfused into peritubular capillaries also increased J_HCO3^–, compared with basal levels during intact capillary perfusion with blood. In addition, in isolated perfused tubules aldosterone causes a transient increase of cytosolic free calcium ([Ca²⁺]_i), monitored fluorometrically. In the presence of ethanol (in similar concentration used to prepare the hormonal solution), spironolactone (10^–6 M, a mineralocorticoid receptor antagonist), actinomycin D (10^–6 M, an inhibitor of gene transcription), or cycloheximide (40 mM, an inhibitor of protein synthesis), the J_HCO3^– and the [Ca²⁺]_i were not different from the control value; these drugs also did not prevent the stimulatory effect of aldosterone on J_HCO3^– and on [Ca²⁺]_i. However, in the presence of RU 486 alone [10^–6 M, a classic glucocorticoid receptor (GR) antagonist], a significant decrease on J_HCO3^– and on [Ca²⁺]_i was observed; this antagonist also inhibited the stimulatory effect of aldosterone on J_HCO3^– and on [Ca²⁺]_i. These studies indicate that luminal or peritubular aldosterone (10^–12 M) has a direct nongenomic stimulatory effect on J_HCO3^– and on [Ca²⁺]_i in proximal tubule and that probably GR participates in this process. The data also indicate that endogenous aldosterone stimulates J_HCO3^– in middle proximal tubule.

S2 bicarbonate reabsorption