Submitted on March 27, 2008
Revised on February 11, 2009
Accepted on February 14, 2009
Direct action of Aldosterone on bicarbonate reabsorption in vivo cortical proximal tubule
Patricia E. Silva-Pergher, Deise Leite-Dellova1, and Margarida de Mello-Aires2*
1 USP
2 University of São Paulo
* To whom correspondence should be addressed. E-mail: mmaires{at}icb.usp.br.
The direct action of aldosterone (10-12 M) on net bicarbonate reabsorption (JHCO3-) was evaluated by stationary microperfusion of in vivo middle proximal tubule (S2) of rat kidney, using H ion-sensitive microelectrodes. Aldosterone in luminally perfused tubules caused a significant increase in JHCO3- from a mean control value of 2,84 ± 0.079 nmol.cm-2.s-1 [49/19 (n° of measurements/n° of tubules)] to 4,20 ± 0,145 nmol.cm-2.s-1 (58/10). Aldosterone perfused into peritubular capillaries also increased JHCO3-, 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 (MR) antagonist], actinomycin D (10-6 M, an inhibitor of gene transcription) or cycloheximide (40 mM, an inhibitor of protein synthesis), the JHCO3- and the [Ca2+]i were not different from the control value; these drugs also did not prevent the stimulatory effect of aldosterone on JHCO3- 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 JHCO3- and on [Ca2+]i were observed; this antagonist also inhibited the stimulatory effect of aldosterone on JHCO3- and on [Ca2+]i . These studies indicate that luminal or peritubular aldosterone (10-12 M) has a direct nongenomic stimulatory effect on JHCO3- and on [Ca2+]i in proximal tubule and that probably GR participates in this process. The data also indicate that endogenous aldosterone stimulates JHCO3- in middle proximal tubule.
