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J Physiol Volume 578, Number 2, 413-424, January 15, 2007 DOI: 10.1113/jphysiol.2006.118315
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CELLULAR

Role of vasopressin in rat distal colon function

Esther Cristià1, Concepció Amat1, Richard J. Naftalin2 and Miquel Moretó1

1 Departament de Fisiologia, Facultat de Farmàcia, Universitat de Barcelona, Barcelona, Spain
2 Physiology Division, King's College London, Guys Campus, London, UK

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 mM NaCl) or a low-Na+ (LS; 150 µM 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), {alpha}-smooth muscle actin ({alpha}-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 {alpha}-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.

(Received 4 August 2006; accepted after revision 26 October 2006; first published online 2 November 2006)
Corresponding author M. Moretó: Departament de Fisiologia, Facultat de Farmàcia, Universitat de Barcelona, Av/Joan XXIII s/n, E-08028 Barcelona, Spain. Email: mmoreto{at}ub.edu







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