Aldosterone mediates the changes in hexose transport induced by low sodium intake in chicken distal intestine.

1. In chickens, low Na+ diets markedly decrease the hexose transport in the rectal segment of the large intestine; transport in the ileum shows a lower, but significant reduction and transport in the jejunum is unaffected. These effects involve both apical (SGLT1) and basolateral (GLUT2) hexose transporters. 2. The role of the renin-angiotensin-aldosterone axis (RAAS) in the epithelial response to Na+ intake was studied in chickens fed high-NaCl (HS) and low-NaCl (LS) diets. The V(max) of alpha-methyl-D-glucoside and D-glucose were determined in vesicles from the brush-border (BBMVs) and basolateral (BLMVs) membranes, respectively. The binding of phlorizin to BBMV and cytochalasin B to BLMV were used as indicators of the abundance of SGLT1 and GLUT2, respectively. 3. In HS-adapted chickens, the serum concentration of aldosterone (means +/- S.E.M.) was 35 +/- 5 pg ml(-1) (n = 6) and that of renin was 20 +/- 2 ng ml(-1) (n = 3). In LS-fed birds, these values were 166 +/- 12 pg ml(-1) (n = 6) and 122 +/- 5 ng ml(-1) (n = 3), respectively. Administration of captopril, the inhibitor of the angiotensin-converting enzyme (ACE), to LS-chickens lowered the aldosterone serum concentration without affecting the renin concentration. Captopril also prevented the reduction of apical and basolateral hexose transport in ileum and rectum characteristic of the intestinal response to LS adaptation. 4. Administration of the aldosterone antagonist spironolactone to LS-adapted chickens did not affect the serum concentrations of aldosterone, but prevented the effects of LS intake on hexose transport in both apical and basolateral membranes. This suggests that the effects of aldosterone are mediated by cytosolic mineralcorticoid receptors. 5. Administration of exogenous aldosterone to HS-fed birds induced hexose transport and binding properties typical of the LS-adapted animals. These findings support the view that aldosterone, besides its primary role in controlling intestinal Na+ absorption, can also modulate the expression of apical and basolateral glucose transporters in the chicken distal intestine.