Aldosterone (Aldo) and Arginine-vasopressin (AVP) can regulate Na and water reabsorption at the crypt colon level (Cristià et al, 2007). Raised Aldo, in response to low NaCl intake, or raised AVP, in response to dehydration, induce pericryptal myofibroblast proliferation in the pericryptal sheath surrounding rat distal colonic crypts with concomitant reduction in colonic crypt wall permeability. We have reproduced these phenomena in vitro, using co-cultures of human CCD-18Co myofibroblasts and T84 colonic epithelial cell lines. Myofibroblast and epithelial cell proliferation was quantified from 5-Bromo-2′-deoxyuridine incorporation, the expression of growth factors (EGF, PDGFA, TGFβ1 and VEGFa) by real-time PCR, and the expression of epithelial junctional proteins (claudin IV, β-catenin) by Western blot. Results (means ± SEM; n=6) were analysed by ANOVA. 24 h incubation with 100 nM Aldo or with 10 nM AVP stimulated myofibroblasts cell proliferation by 70% and 60%, respectively. Aldo stimulated the myofibroblast expression of EGF by 30%, (p<0.05) and PDFGA (28%, p<0.05); while AVP increased myofibroblast PDGFA expression by 32%, (p<0.05). The AVP induced effects were prevented when Manning peptide, a V1 receptor antagonist, and Tolvaptan, a V2 receptor antagonist, were present in the incubation medium, and the effects of Aldo were prevented by spironolactone. Conditioned medium from myofibroblasts incubated with either Aldo or AVP, stimulated cell proliferation in T84 cells (42% and 54%, respectively; p<0.05), and both hormones increased 24-34% the expression of claudin IV and β-catenin (p<0.05). These results indicate that changes in colonic permeability during dehydration in response to raised AVP are mediated by PDGFA secreted by myofibroblasts; whereas the similar changes in colonic epithelial cell permeability induced by increase in Aldo induced by a low salt diet are mediated by myofibroblast secreted EGF and PDGFA.