UNLABELLED: It has been reported that PCMBS (p-chloromercuribenzene sulfonate) blocks the water permeability of red cells and of the tubular kidney membranes. In this study we compare the effects of this mercurial compound on the permeability of water and other small solutes in the frog urinary bladder. We observed that: (i) 5 mM PCMBS applied at pH 5.0 to the mucosal side inhibited the net and unidirectional water fluxes induced by oxytocin without changing the delta Pf/delta Pd ratio. (ii) The oxytocin-induced urea and Na+ influxes were also inhibited by PCMBS. (iii) The unidirectional Cl- movement was first reduced and then increased during the course of PCMBS treatment. (iv) The short-circuit measured at low mucosal Na+ concentration (10 mM), diminished continuously, whereas the transepithelial resistance first increased and then diminished. (v) Mannitol, raffinose, alpha-methyl-glucose, antipyrine, caffeine and Rb+ movements were not changed significantly during the first 26 min of the water permeability inhibition. IN CONCLUSION: (i) The ADH-sensitive water, urea and Na+ transport systems were inhibited by PCMBS, (ii) PCMBS did not induce a nonspecific and general effect on the permeability of the membrane during the development of the water permeability inhibition, and (iii) in terms of water channels, the inhibition of water transport with the maintenance of a high Pf/Pd ratio suggests that PCMBS closes the water channels in an all or none manner, reducing their operative number in the apical border of frog bladder.
UNLABELLED: It has been reported that PCMBS (p-chloromercuribenzene sulfonate) blocks the water permeability of red cells and of the tubular kidney membranes. In this study we compare the effects of this mercurial compound on the permeability of water and other small solutes in the frog urinary bladder. We observed that: (i) 5 mM PCMBS applied at pH 5.0 to the mucosal side inhibited the net and unidirectional water fluxes induced by oxytocin without changing the delta Pf/delta Pd ratio. (ii) The oxytocin-induced urea and Na+ influxes were also inhibited by PCMBS. (iii) The unidirectional Cl- movement was first reduced and then increased during the course of PCMBS treatment. (iv) The short-circuit measured at low mucosal Na+ concentration (10 mM), diminished continuously, whereas the transepithelial resistance first increased and then diminished. (v) Mannitol, raffinose, alpha-methyl-glucose, antipyrine, caffeine and Rb+ movements were not changed significantly during the first 26 min of the water permeability inhibition. IN CONCLUSION: (i) The ADH-sensitive water, urea and Na+ transport systems were inhibited by PCMBS, (ii) PCMBS did not induce a nonspecific and general effect on the permeability of the membrane during the development of the water permeability inhibition, and (iii) in terms of water channels, the inhibition of water transport with the maintenance of a high Pf/Pd ratio suggests that PCMBS closes the water channels in an all or none manner, reducing their operative number in the apical border of frog bladder.