Role of vasopressin in rat distal colon function

The specific role of vasopressin in colonic crypt function and its possible synergistic action with aldosterone were studied. Sprague-Dawley rats fed a high-Na⁺ (HS; 150 m m NaCl) or a low-Na⁺ (LS; 150 μ m NaCl) diet were deprived of water or infused with vasopressin, and some animals were treated with specific vasopressin receptor subtype V₁ and V₂ antagonists. The expression of the epithelial Na⁺ channel (ENaC), α-smooth muscle actin (α-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 fluorescent dye (sodium red) and crypt permeability was measured by the rate of escape of fluorescein isothiocyanate-labelled dextran (10 kDa) from the crypt lumen into the pericryptal space in isolated rat distal colonic mucosa. A high plasma concentration of vasopressin raised α-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 blockade 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 action of vasopressin 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 myofibroblast growth which affects crypt absorption, and these effects are independent of the presence of aldosterone.