The nature of the neutral Na+−Cl− coupled entry at the apical membrane of rabbit gallbladder epithelium: III. Analysis of transports on membrane vesicles

1990 ◽  
Vol 118 (2) ◽  
pp. 107-120 ◽  
Author(s):  
Giuliano Meyer ◽  
Guido Bottà ◽  
Carlo Rossetti ◽  
Dario Cremaschi
Keyword(s):  
Apical Membrane ◽  
Membrane Vesicles ◽  
Gallbladder Epithelium ◽  
Rabbit Gallbladder

Transcellular sodium transport and intracellular sodium activities in rabbit gallbladder

1986 ◽  
Vol 251 (1) ◽  
pp. G155-G159
Author(s):  
W. M. Moran ◽  
R. L. Hudson ◽  
S. G. Schultz
Keyword(s):  
Small Intestine ◽  
Apical Membrane ◽  
Basolateral Membrane ◽  
Gallbladder Epithelium ◽  
Na Transport ◽  
Twofold Increase ◽  
Average Value ◽  
Intracellular Na Activity ◽  
Rabbit Gallbladder ◽  
Sustained Increase

This study was designed to explore the relation between the rate of transcellular active Na+ transport by rabbit gallbladder epithelium, JNa, and the intracellular Na+ activity, (Na)c; the latter was determined by use of highly selective Na+ microelectrodes. The underlying strategy was based on the well-established observation that JNa is stimulated by the presence of bicarbonate in the bathing solutions. Our results confirm previous observations that the addition of bicarbonate to the bathing solutions results in a twofold increase in JNa. In the absence of bicarbonate, (Na)c averaged 16 mM. Within 2–4 min after the addition of bicarbonate to both bathing solutions, (Na)c increased to an average value of 22 mM and then gradually declined and by 15 min did not differ significantly from the value observed in the absence of bicarbonate. Thus, a twofold increase in JNa is not associated with an increase in (Na)c. These results are in accord with earlier observations on Necturus urinary bladder and small intestine and contradict the notion that an increase in the rate of active Na+ extrusion from the cell across the basolateral membrane in response to an increase in the rate of Na+ entry across the apical membrane is necessarily the result of a sustained increase in (Na)c.

Localization of Sodium in Normal and Inhibited Transporting Epithelia

1971 ◽  
Vol 29 ◽  
pp. 392-393
Author(s):  
G. I. Kaye ◽  
J. D. Cole
Keyword(s):  
Plasma Membrane ◽  
Similar Pattern ◽  
Fixation Method ◽  
Colonic Epithelium ◽  
Gallbladder Epithelium ◽  
Rabbit Colon ◽  
Rabbit Gallbladder

For a number of years we have used an adaptation of Komnick's KSb(OH)6-OsO4 fixation method for the localization of sodium in tissues in order to study transporting epithelia under a number of different conditions. We have shown that in actively transporting rabbit gallbladder epithelium, large quantities of NaSb(OH)6 precipitate are found in the distended intercellular compartment, while localization of precipitate is confined to the inner side of the lateral plasma membrane in inactive gallbladder epithelium. A similar pattern of distribution of precipitate has been demonstrated in human and rabbit colon in active and inactive states and in the inactive colonic epithelium of hibernating frogs.

scholarly journals Electrophysiological effects of basolateral [Na+] in Necturus gallbladder epithelium.

1992 ◽  
Vol 99 (2) ◽  
pp. 241-262 ◽  
Author(s):  
G A Altenberg ◽  
J S Stoddard ◽  
L Reuss
Keyword(s):  
Apical Membrane ◽  
Basolateral Membrane ◽  
Membrane Resistance ◽  
Membrane Voltage ◽  
Gallbladder Epithelium ◽  
K Channels ◽  
Necturus Gallbladder ◽  
Electrophysiological Effects ◽  
Paracellular Diffusion ◽  
Cl Conductance

In Necturus gallbladder epithelium, lowering serosal [Na+] ([Na+]s) reversibly hyperpolarized the basolateral cell membrane voltage (Vcs) and reduced the fractional resistance of the apical membrane (fRa). Previous results have suggested that there is no sizable basolateral Na+ conductance and that there are apical Ca(2+)-activated K+ channels. Here, we studied the mechanisms of the electrophysiological effects of lowering [Na+]s, in particular the possibility that an elevation in intracellular free [Ca2+] hyperpolarizes Vcs by increasing gK+. When [Na+]s was reduced from 100.5 to 10.5 mM (tetramethylammonium substitution), Vcs hyperpolarized from -68 +/- 2 to a peak value of -82 +/- 2 mV (P less than 0.001), and fRa decreased from 0.84 +/- 0.02 to 0.62 +/- 0.02 (P less than 0.001). Addition of 5 mM tetraethylammonium (TEA+) to the mucosal solution reduced both the hyperpolarization of Vcs and the change in fRa, whereas serosal addition of TEA+ had no effect. Ouabain (10(-4) M, serosal side) produced a small depolarization of Vcs and reduced the hyperpolarization upon lowering [Na+]s, without affecting the decrease in fRa. The effects of mucosal TEA+ and serosal ouabain were additive. Neither amiloride (10(-5) or 10(-3) M) nor tetrodotoxin (10(-6) M) had any effects on Vcs or fRa or on their responses to lowering [Na+]s, suggesting that basolateral Na+ channels do not contribute to the control membrane voltage or to the hyperpolarization upon lowering [Na+]s. The basolateral membrane depolarization upon elevating [K+]s was increased transiently during the hyperpolarization of Vcs upon lowering [Na+]s. Since cable analysis experiments show that basolateral membrane resistance increased, a decrease in basolateral Cl- conductance (gCl-) is the main cause of the increased K+ selectivity. Lowering [Na+]s increases intracellular free [Ca2+], which may be responsible for the increase in the apical membrane TEA(+)-sensitive gK+. We conclude that the decrease in fRa by lowering [Na+]s is mainly caused by an increase in intracellular free [Ca2+], which activates TEA(+)-sensitive maxi K+ channels at the apical membrane and decreases apical membrane resistance. The hyperpolarization of Vcs is due to increase in: (a) apical membrane gK+, (b) the contribution of the Na+ pump to Vcs, (c) basolateral membrane K+ selectivity (decreased gCl-), and (d) intraepithelial current flow brought about by a paracellular diffusion potential.

Different sodium chloride cotransport systems in the apical membrane of rabbit gallbladder epithelial cells

1983 ◽  
Vol 73 (3) ◽  
pp. 227-235 ◽  
Author(s):  
Dario Cremaschi ◽  
Giuliano Meyer ◽  
Sandra Bermano ◽  
Maurizia Marcati
Keyword(s):  
Sodium Chloride ◽  
Epithelial Cells ◽  
Apical Membrane ◽  
Rabbit Gallbladder ◽  
Cotransport Systems
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