â-Cyclodextrin and permeability to water in the bladder of Bufo arenarum.

ORCE G.; CASTILLO G.,; CHANAMPA Y.

CANADIAN JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY

NATL RESEARCH COUNCIL CANADA-N R C RESEARCH PRESS

Lugar: Otawa; Año: 2011 vol. 89 p. 311 - 315

0008-4212

We measured the effect of beta-cyclodextrin, (BCD, a cholesterol scavenger) on water flow across the isolated toad bladder exposed to an osmotic gradient (Jw) by a gravimetric technique. BCD, when present in the solution bathing the apical side of the bladder, inhibited the increase in Jw caused by nystatin, a polyene antibiotic which binds cholesterol forming water channels across the apical membrane. The increase in Jw caused by oxytocin (which stimulates de synthesis of cAMP), however, was not modified by apical BCD. In contrast, when present in the serosal bath, BCD inhibited Jw in the oxytocin-treated bladder but did not alter the response to theophylline (an inhibitor of cyclic nucleotide phosphodiesterase). The present data are consistent with the notion that agents that increase Jw by interacting with membrane receptors (which have been suggested to cluster in cholesterol-rich domains of the membrane) are selectively altered by BCD-mediated cholesterol extraction from the cell membrane, whereas agents that do not interact with receptors or other membrane components appear not to be affected by alteration of the membrane lipid environment. water flow across the isolated toad bladder exposed to an osmotic gradient (Jw) by a gravimetric technique. BCD, when present in the solution bathing the apical side of the bladder, inhibited the increase in Jw caused by nystatin, a polyene antibiotic which binds cholesterol forming water channels across the apical membrane. The increase in Jw caused by oxytocin (which stimulates de synthesis of cAMP), however, was not modified by apical BCD. In contrast, when present in the serosal bath, BCD inhibited Jw in the oxytocin-treated bladder but did not alter the response to theophylline (an inhibitor of cyclic nucleotide phosphodiesterase). The present data are consistent with the notion that agents that increase Jw by interacting with membrane receptors (which have been suggested to cluster in cholesterol-rich domains of the membrane) are selectively altered by BCD-mediated cholesterol extraction from the cell membrane, whereas agents that do not interact with receptors or other membrane components appear not to be affected by alteration of the membrane lipid environment. beta-cyclodextrin, (BCD, a cholesterol scavenger) on water flow across the isolated toad bladder exposed to an osmotic gradient (Jw) by a gravimetric technique. BCD, when present in the solution bathing the apical side of the bladder, inhibited the increase in Jw caused by nystatin, a polyene antibiotic which binds cholesterol forming water channels across the apical membrane. The increase in Jw caused by oxytocin (which stimulates de synthesis of cAMP), however, was not modified by apical BCD. In contrast, when present in the serosal bath, BCD inhibited Jw in the oxytocin-treated bladder but did not alter the response to theophylline (an inhibitor of cyclic nucleotide phosphodiesterase). The present data are consistent with the notion that agents that increase Jw by interacting with membrane receptors (which have been suggested to cluster in cholesterol-rich domains of the membrane) are selectively altered by BCD-mediated cholesterol extraction from the cell membrane, whereas agents that do not interact with receptors or other membrane components appear not to be affected by alteration of the membrane lipid environment.