Abstract.
The involvement of enzymes catabolizing hyaluronic acid (hyaluronidase, β-glucuronidase, N-acetyl-β-D-hexosaminidase) in the hydroosmotic effect of vasopressin in the frog (Rana ridibunda) urinary bladder was studied. It was observed that vasopressin (50 nM), an agonist of V2 receptors, L-desamino-8-D-arginine-vasopressin (dDAVP, 1.5 µM) and forskolin (30 µM) activated the enzymes and caused their release into Ringer solution at the mucosal side, together with an increase in osmotic water flow. The effect of AVP on enzyme activity developed 10 min after the hydroosmotic response. Cytochalasin B (a specific inhibitor of actin filament elongation, 50 nM) blocked the hydroosmotic response to AVP; hyaluronate hydrolase activity increased in the bladder tissue but not in Ringer solution. It is suggested that the involvement of hyaluronate hydrolases in AVP's effect is mediated by a cAMP-dependent mechanism and provides favorable conditions for an increase in the permeability of glycosaminoglycan structures adjacent to the apical cell surface.
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Ivanova, L., Melidi, N. Effects of vasopressin on hyaluronate hydrolase activities and water permeability in the frog urinary bladder. Pflügers Arch - Eur J Physiol 443, 72–77 (2001). https://doi.org/10.1007/s004240100575
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DOI: https://doi.org/10.1007/s004240100575