Role of corticosteroids in distal acidification of amiloride-treated rats

Abstract

The role of amiloride-dependent sodium channels in the action of adrenal cortical steroids on urine–blood [Formula: see text] (U–B [Formula: see text]) differences was studied in bicarbonate-infused and amiloride-treated adrenalectomized rats. U–B [Formula: see text] was significantly reduced by amiloride in bicarbonate-infused control rats. Adrenalectomy further reduced U–B [Formula: see text] in amiloride-treated, bicarbonate-infused rats (from 27.9 ± 1.82 mmHg in sham-operated rats to 21.3 ± 1.58 mmHg in adrenalectomized (ADX) rats) (1 mmHg = 133.322 Pa). Acute administration of corticosterone and 18-hydroxycorticosterone (18-OH-B), but not of aldosterone, caused recovery of U–B [Formula: see text] to the level of sham-operated animals treated with amiloride. Aldosterone did not affect U–B [Formula: see text] in the presence of amiloride (21.9 mmHg ADX group vs. 20.98 mmHg aldosterone group). Results are compatible with aldosterone affecting distal H ion secretion mostly by a sodium and potential difference dependent mechanism, while corticosterone and 18-OH-B should act by other mechanisms (e.g., increased luminal buffer level).Key words: distal H ion secretion, corticosteroids, amiloride, adrenalectomy, aldosterone, corticosterone, 18-hydroxycorticosterone.