Lidocaine blockage of basolateral potassium channels in the amphibian urinary bladder.

Driessche, Willy Van

doi:10.1113/jphysiol.1986.sp016344

Cited by 26 publications

(12 citation statements)

References 30 publications

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“…Such situations could be achieved by permeabilizing the apical membrane with an ionophore [6,21]. This treatment results in the appearance of two semicircles in the Nyquist plot, each of them reflecting the properties of the apical and basolateral membranes.…”

Section: Preparationmentioning

confidence: 99%

Transepithelial capacitance decrease reveals closure of lateral interspace in A6 epithelia

Driessche¹,

Vos

Jans³

et al. 1999

Pfl�gers Archiv European Journal of Physiology

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A sine wave method was used to measure transepithelial capacitance (CT) at 4.1 kHz (CHFT ). Model calculations show that CHFT reflects the equivalent capacitance of the series arrangement of apical and basolateral membrane capacitance. Cell swelling induced by reducing the basolateral osmolality from 260 to 140 mosmol/kg H2O (NaCl or sucrose removal) transiently decreased CHFT. The decrease in CHFT (DeltaCHFT ) reached its maximum 30 s after the onset of cell swelling and a complete recovery of CHFT was attained within 3-4 min. DeltaCHFT could be diminished by manoeuvres that reduced the rate or amplitude of cell swelling, i.e. lowering the temperature or treatment with low concentrations of glutaraldehyde (0.025%). DeltaCHFT increased with the magnitude of the osmotic perturbation but saturated at large volume expansions. DeltaCHFT increased with culture time. Electron micrographs showed a clear correlation between time course of CHFT changes and the closure of the lateral interspace (LIS). A striking correlation between the occurrence of CHFT recovery and the ability of the cells to develop a regulatory volume decrease (RVD) was found: Gd3+ (0.5 mM) inhibited both phenomena. The frequency dependence of CT was obtained from impedance spectra recorded over the range of 4 Hz to 22 kHz. These data agree with model calculations in which the contribution of the access resistance to the lateral membrane was included. All observations are consistent with the idea that DeltaCHFT originates from the closure of the LIS during cell swelling. The latter phenomenon increases the access resistance to the lateral membrane, which results in a marked reduction of the basolateral membrane area detected at high frequencies with capacitance measurements.

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Section: Preparationmentioning

confidence: 99%

Transepithelial capacitance decrease reveals closure of lateral interspace in A6 epithelia

Driessche¹,

Vos

Jans³

et al. 1999

Pfl�gers Archiv European Journal of Physiology

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“…As shown in Fig. 3, dexamethasone produced a slow increase in 1SC that reached & Erlij, 1988;Van Driessche, 1986) showed that as the apical membrane is progressively shunted by nystatin the impedance data pass first through an intermediate period in which they 1986). For these experiments the apical side of the epithelia was perfused with a solution in which K+ was the major monovalent cation.…”

Section: Apical Membrane Capacitancementioning

confidence: 99%

“…A single time constant is observed in the impedance plots of tight epithelia because CD is much larger than CQ while the apical membrane resistance (Ra) is larger than the basolateral membrane resistance (Rb) (Van Driessche, 1986;Granitzer, Leal, Nagel & Crabbe, 1991a;Wills, Purcell & Clausen, 1992). A particularly important consequence of these relationships is that the measurements of Cm reflect almost exclusively the value of Ca because transepithelial capacitance is related to apical and basolateral capacitance by:…”

Section: Apical Membrane Capacitancementioning

confidence: 99%

Effect of insulin on area and Na+ channel density of apical membrane of cultured toad kidney cells.

Erlij

Smet

Driessche

1994

The Journal of Physiology

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1. The stimulation of transepithelial Na+ transport caused by insulin in A6 cultured toad kidney cells was investigated by determination of membrane capacitance (Cm), short circuit current (Isc) and current fluctuation analysis. Values of Cm are proportional to membrane area while blocker‐induced current fluctuation analysis provides an estimate of the number of active amiloride‐sensitive Na+ channels in the apical membrane. 2. Insulin simultaneously increased Cm, Isc and Gt (transepithelial conductance) in epithelia incubated with Na(+)‐containing solutions on both sides. 3. Analysis of 6‐chloro‐3,5‐diaminopyrazine‐2‐carboxamide (CDPC)‐induced noise showed that insulin increased the number of active Na+ channels in the apical membrane, without altering the single channel current. 4. When nystatin was used to permeabilize the apical membrane the impedance data revealed the presence of a second time constant. Analysis of these data indicated that the basolateral membrane capacitance (Cb) is much larger than the apical membrane capacitance (Ca). Insulin administered to nystatin‐treated epithelia increased the values for both capacitances. 5. We suggest that the stimulation of transepithelial Na+ transport caused by insulin may be associated with the exocytotic delivery of transporters to the apical membrane.

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“…In experimental studies in rats, either intravenous or intraalveolar lidocaine reduced fluid clearance in rats by 50% (189). Because lidocaine did not inhibit ENaC when expressed in oocytes, it seems that the inhibitory effect on vectorial fluid transport was primarily on the basal surface of alveolar epithelial cells, either through an effect on the activity of Na ϩ -K ϩ -ATPase or through an indirect effect through blockade of potassium channels, a wellknown property of lidocaine (47,156,302,357). The effect of lidocaine was completely reversible with ␤ 2 -agonist therapy (189).…”

Section: Anestheticsmentioning

confidence: 99%

Lung Epithelial Fluid Transport and the Resolution of Pulmonary Edema

Matthay

Folkesson²,

Clérici³

2002

Physiological Reviews

610

649

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The discovery of mechanisms that regulate salt and water transport by the alveolar and distal airway epithelium of the lung has generated new insights into the regulation of lung fluid balance under both normal and pathological conditions. There is convincing evidence that active sodium and chloride transporters are expressed in the distal lung epithelium and are responsible for the ability of the lung to remove alveolar fluid at the time of birth as well as in the mature lung when pathological conditions lead to the development of pulmonary edema. Currently, the best described molecular transporters are the epithelial sodium channel, the cystic fibrosis transmembrane conductance regulator, Na+-K+-ATPase, and several aquaporin water channels. Both catecholamine-dependent and -independent mechanisms can upregulate isosmolar fluid transport across the distal lung epithelium. Experimental and clinical studies have made it possible to examine the role of these transporters in the resolution of pulmonary edema.

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Lidocaine blockage of basolateral potassium channels in the amphibian urinary bladder.

Cited by 26 publications

References 30 publications

Transepithelial capacitance decrease reveals closure of lateral interspace in A6 epithelia

Transepithelial capacitance decrease reveals closure of lateral interspace in A6 epithelia

Effect of insulin on area and Na+ channel density of apical membrane of cultured toad kidney cells.

Lung Epithelial Fluid Transport and the Resolution of Pulmonary Edema

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