Aldosterone appears to exert rapid effects via non-genomic mechanisms in addition to its classical genomic actions. Contrary to its well known genomic action on urinary sodium reabsorption and potassium excretion, we have previously shown that aldosterone causes a rapid increase in urinary sodium excretion but has no effect on potassium output in the rat in vivo (Rad et al. 2002). Aldosterone has also been shown to inhibit bicarbonate absorption via a non-genomic pathway in the thick ascending limb in vitro (Good et al. 2002). Accordingly, the aim of this study was to determine whether aldosterone stimulates rapid changes in urinary bicarbonate excretion and urine pH in vivo.

Under Intraval anaesthesia (100 mg kg^-1 sodium thiopentone), male Sprague-Dawley rats received euvolaemic fluid replacement (2.5 % dextrose) of spontaneous urine output using a servo-controlled system (Burgess et al. 1993). After a 3 h equilibration period, control urine and plasma samples were taken, following which half of the animals received aldosterone (42 pmol min^-1) for 1 h before returning to dextrose alone for the final hour. Animals were humanely killed at the end of the experiment.

Aldosterone infusion had no effect on urine flow rate, but resulted in a significant (P < 0.05), rapid increase in urinary sodium excretion (Table 1). Urinary bicarbonate excretion and urine pH did not change over the hour of aldosterone infusion by comparison with control animals. While these data do not provide evidence that aldosterone exerts a rapid effect on urinary pH and bicarbonate excretion in vivo, this possibility cannot be excluded due to potential modification or buffering of the final urine downstream of the thick ascending limb. The natriuresis observed following aldosterone infusion confirms our previous observation (Rad et al. 2002).