The specific role of vasopressin on colonic crypt function and its possible synergistic action with aldosterone were studied. Sprague Dawley rats fed a high-Na+ (HS; 150 mM NaCl) or a low-Na+ (LS; 150 µM NaCl) diet were water deprived or infused with vasopressin and some animals treated with specific V1 and V2 vasopressin receptor subtypes antagonists. The expression of epithelial Na+ channel (ENaC), -smooth muscle actin (-SMA) and aquaporin-2 (AQP-2) were determined by immunolocalization in distal colonic mucosa. The pericryptal Na+ concentration was determined by confocal microscopy, using a low-affinity Na+-sensitive fluorescence dye (Sodium red) and crypt permeability was measured by the rate of escape of FITC-labeled dextran (10 kDa) from the crypt lumen into the pericryptal space in isolated rat distal colonic mucosa. High vasopressin plasma concentration raised -SMA expression in the pericryptal sheath (P<0.05), increased the pericryptal Na+ accumulation in this space (P<0.01) and caused a reduction of crypt wall permeability (P<0.01). All these effects were reversed by selective blocking of V1 and V2 receptors. No synergistic effects with aldosterone were observed. Dehydration and vasopressin infusion increased AQP-2 expression in distal colonic mucosa (P<0.05). This vasopressin action was prevented by Tolvaptan, a specific V2 receptor antagonist (P<0.05). It is concluded that vasopressin has trophic effects in the rat distal colon, increasing pericryptal myofibroblasts growth that affects crypts absorption, and these effects are independent of the presence of aldosterone.