title: Effect of hyperosmotic challenge on basolateral membrane potential in rabbit urinary bladder.
abstract: In the rabbit urinary bladder, serosal hyperosmotic challenge (SHOC) with either 33 mM NaCl or 66 mM mannitol caused basolateral membrane potential (Vbl) to initially depolarize from -52.6 +/- 1.6 to -48.4 +/- 1.4 mV, followed by a recovery of Vbl to -57.5 +/- 1.3 mV after 13.7 +/- 1.0 min. The voltage recovery was dependent on both serosal HCO3- and Cl-, and in the absence of both, Vbl depolarized to -11.6 +/- 1.5 mV and the ratio of apical-to-basolateral resistance (Ra/Rbl) decreased from 21.0 +/- 3.4 to 8.3 +/- 3.1. This decrease in Ra/Rbl and consequent depolarization of Vbl is caused by a decrease in basolateral K+ conductance. Replacement of serosal Cl- with NO3- or SCN- followed by SHOC caused a sustained depolarization of Vbl to -32.5 +/- 4.4 and -40.9 +/- 0.9 mV, respectively. However, when Br- was used to replace Cl-, voltage recovery occurred but was slowed (24.0 +/- 2.7 min) and reduced in magnitude (-47.5 +/- 3.5 mV). Addition of amiloride (1 mM) or niflumic acid (100 microM), but not bumetanide (1 microM), to the serosal bathing solution inhibited voltage recovery causing Vbl to depolarize to -36.3 +/- 2.6 and -41.5 +/- 4.5 mV, respectively. Serosal addition of ouabain after SHOC caused Vbl to depolarize by 10.8 +/- 0.9 mV in 2 min. We speculate that the SHOC-induced initial depolarization of Vbl is a loss of Ba2(+)-sensitive K+ conductance caused by cell shrinkage. The subsequent repolarization/hyperpolarization of Vbl is caused by an enhanced basolateral membrane Na+ pump current and a reappearance of the Ba2(+)-sensitive K+ conductance. The parallel operation of Na(+)-H+ and Cl(-)-HCO3- exchanges will then supply Na+ for the pump current and, via cellular accumulation of Na+, K+, and Cl-, might result in a partial recovery of cell volume and thus Ba2(+)-sensitive K+ conductance.
authors.affiliation: Department of Physiology and Biophysics, University of Texas Medical Branch, Galveston 77550.
authors.forename: P J
authors.initials: PJ
authors.lastname: Donaldson
authors.forename: S A
authors.initials: SA
authors.lastname: Lewis
mesh_terms: D000584:Amiloride / Q000494:pharmacology; D000818:Animals; D000838:Anions; D002034:Bumetanide / Q000494:pharmacology; D002462:Cell Membrane / Q000187:drug effects / Q000502:physiology*; D002712:Chlorides / Q000378:metabolism; D005942:Gluconates / Q000494:pharmacology; D006982:Hypertonic Solutions; D066298:In Vitro Techniques; D007700:Kinetics; D008297:Male; D008353:Mannitol / Q000494:pharmacology; D008564:Membrane Potentials / Q000187:drug effects; D009092:Mucous Membrane / Q000187:drug effects / Q000502:physiology; D009544:Niflumic Acid / Q000494:pharmacology; D010042:Ouabain / Q000031:analogs & derivatives / Q000494:pharmacology; D011817:Rabbits; D012965:Sodium Chloride / Q000494:pharmacology; D001743:Urinary Bladder / Q000502:physiology*
chemical_list: D000838:Anions; D002712:Chlorides; D005942:Gluconates; D006982:Hypertonic Solutions; D002034:Bumetanide; C000977:dihydroouabain; D008353:Mannitol; D012965:Sodium Chloride; D009544:Niflumic Acid; D010042:Ouabain; D000584:Amiloride; C030691:gluconic acid