Interactions of sodium transport, cell volume, and calcium in frog urinary bladder.

Davis, C. William; Finn, Arthur L.

doi:10.1085/jgp.89.5.687

Cited by 47 publications

(17 citation statements)

References 34 publications

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“…From the dependence of the RVD on extracellular Ca2 , it is conceivable that the Ca2+ ions may originate from the extracellular space in the case of human lymphocytes 698 VOLUME-REGULATORY K+ AND Cl-CHANNELS (Sarkadi et al 1984b) and frog urinary bladder (Wong & Chase, 1986;Davis & Finn, 1987). On the other hand, Ca2" ions released from some intracellular stores could be responsible for the RVD in duck erythrocytes (Kregenow, 1971), Ehrlich ascites tumour cells (Hoffmann et al 1984) and MDCK cells (Roy & Sauve, 1987), since the RVD was independent of the extracellular Ca2" in these cells.…”

Section: (C) Intracellularmentioning

confidence: 99%

“…Whether the volume-regulatory ion channels are located on the luminal or basolateral membrane is not clear from the present study, since the electrical recordings were made at the whole-cell level in Intestine 407 cells and the cell is rather an undifferentiated cell line lacking the polarity. In a variety of epithelia, however, volume-regulatory KCl exit pathways were suggested to reside in the basolateral membrane (Larson & Spring, 1984;Lau et al 1984;Davis & Finn, 1987).…”

Section: (C) Intracellularmentioning

confidence: 99%

“…Several lines of circumstantial evidence have suggested that activation of volume-regulatory K+ transport systems is controlled by cytosolic Ca2+ ions (Grinstein, Dupre & Rothstein, 1982b;Cala, 1983;Hoffmann et al 1984;Foskett & Spring, 1985;Sarkadi, Cheung, Mack, Grinstein, Gelfand & Rothstein, 1985;Davis & Finn, 1987). Hoffmann, Lambert & Simonsen (1986) have raised the possibility that cytosolic Ca2+ ions are also involved in the activation of volume-regulatory Cl-channels during the RVD since activation of Cl-transport is induced not only during the RVD but also upon A23187-induced shrinkage of Ehrlich ascites tumour cells.…”

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Ca2+ sensitivity of volume‐regulatory K+ and Cl‐ channels in cultured human epithelial cells.

Hazama

Okada

1988

The Journal of Physiology

224

166

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SUMMARY1. During exposure to a hypotonic solution, cultured human epithelial cells (Intestine 407) exhibited a regulatory volume decrease (RVD) after initial osmotic swelling.2. The volume readjustment was slowed by elevating the extracellular K+ concentration and facilitated by reducing the extracellular Cl-concentration. Not only putative K+ channel blockers, quinine and Ba2", but also a stilbene derivative Cl-channel blocker (SITS) inhibited the RVD.3. The volume recovery of hypoosmotically swollen cells was very much suppressed by the deprivation of extracellular Ca2+ ions or by chelation of cytosolic Ca2+ ions with Quin-2 loaded within the cells.4. Biphasic membrane potential changes were associated with the RVD process at low extracellular K+ and Cl-concentrations. The initial hyperpolarizing response was inhibited by quinine and Ba2 , whereas the late depolarizing response was inhibited by SITS. The deprivation of extracellular Ca21 inhibited the initial hyperpolarizing phase but not the late depolarizing phase.5. Two-microelectrode voltage clamp studies showed that the initial hyperpolarization and late depolarization were associated with quinine-sensitive outward currents and SITS-sensitive inward currents, respectively. The reversal potentials estimated from the current-voltage curves were about -80 mV for the initial response and -27 mV for the late response. Tenfold changes in the K+ and C1-concentrations shifted these reversal potentials by 50 mV for the initial response and by 42 mV for the late response.6. Under whole-cell recordings, similar current changes were observed in the cells exposed to a hypotonic solution, when the intracellular Ca2+ ions were moderately buffered with 1 mM-EGTA in the dialysing solution filled in a patch pipette. When most Ca2+ ions were chelated with 10 mM-EGTA in the pipette solution, the initial outward current as well as the corresponding hyperpolarization was suppressed, but the late current associated with the depolarizing phase was preserved.7. Intracellular Ca21 injections induced an increase in the quinine-sensitive K+ conductance but failed to activate the Cl-conductance.8. It is concluded that both K+ and Cl-channels are involved in the regulatory volume decrease, and that the former channel is exclusively activated by elevation of the cytosolic Ca2+ concentration in the epithelial cells.

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Section: (C) Intracellularmentioning

confidence: 99%

Section: (C) Intracellularmentioning

confidence: 99%

mentioning

confidence: 99%

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Ca2+ sensitivity of volume‐regulatory K+ and Cl‐ channels in cultured human epithelial cells.

Hazama

Okada

1988

The Journal of Physiology

224

166

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“…In the experiments of Davis and Finn [ 10,12], external Ca2+ was necessary for RVD. Further, inhibition of apical membrane Na4 entry with amiloride and block of basolateral Na4 extrusion with the cardioactive steroid ouabain did not cause measurable changes in cell volume under control conditions.…”

Section: Volume Regulation In Tight Epitheliamentioning

confidence: 99%

Cell Volume Regulation in Nonrenal Epithelia

Reus

1988

Kidney Blood Press Res

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Cell volume regulation occurs in both tight, Na⁺-transporting epithelia (e.g., frog skin) and in leaky, NaCl-transporting epithelia (e.g., amphibian gallbladder). In tight epithelia volume regulation occurs only in response to cell swelling, i.e. only regulatory volume decrease (RVD) is observed, whereas in leaky epithelia cell volume regulation has been observed in response to osmotic challenges that either swell or shrink the cells. In other words, both RVD and regulatory volume increase (RVI) are present. Both volume regulatory responses involve stimulation of ion transport in a polarized fashion: in RVD the response is basolateral KC1 efflux, whereas in RVI it is apical membrane NaCl uptake. The loss of KCl during RVD appears to result in most instances from increases in basolateral electrodiffusive K⁺ and Cl^- permeabilities. In gallbladder, concomitant activation of coupled KCl efflux may also occur. The RVI response includes activation of apical membrane cation (Na⁺/H⁺) and anion (Cl^-/HCO^-₃) exchangers. It is presently unclear whether the net ion fluxes resulting from activation of these transporters, during either RVD or RVI, account for the measured rates of restoration of cell volume. In gallbladder epithelium, RVD is inhibited by agents which disrupt microfilaments or interfere with the Ca²⁺-calmodulin system. These pharmacologic effects are absent in RVI. Some steps in the chain of events resulting in either RVI or RVD have been established, but the signals involved remain largely unknown. There is reason to suspect a role of intracellular pH in the case of RVI and of membrane insertion of transporters in the case of RVD, possibly with causal roles of both intracellular Ca²⁺ and the cytoskeleton in the latter.

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“…The mechanisms of osmoregulatory K ϩ and Cl Ϫ efflux have not been completely understood. However, K ϩ and Cl Ϫ channels have been proposed to play an important role in RVD in various kinds of cells, such as those in frog urinary bladder [4], human lymphocytic cells [5], human epithelial cells [6], human platelets [7], and epithelial cells of frog skin [8].…”

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The Involvement of Calcium Mobilization in the Calcium-Activated Potassium Currents Activated by Hyposmotic Swelling in Gastric Antral Circular Myocytes of the Guinea-Pig.

Piao

Liu²,

Lin³

et al. 2001

JJP

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The cells of vertebrates exposed to hyposmotic media, initially swell by osmotic water equilibration, but subsequently regulate their volume (regulatory volume decrease, RVD) by a loss of KCl and water (for review, see references [1][2][3]). The mechanisms of osmoregulatory K ϩ and Cl Ϫ efflux have not been completely understood. However, K ϩ and Cl Ϫ channels have been proposed to play an important role in RVD in various kinds of cells, such as those in frog urinary bladder [4], human lymphocytic cells [5], human epithelial cells [6], human platelets [7], and epithelial cells of frog skin [8].Both extracellular and intracellular [Ca 2ϩ ] are too low in animals to be useful as osmolytes. However, the Ca 2ϩ role during RVD has been recognized for many years. Many patch-clamp studies have found that the activation of volume-regulatory K ϩ channels is controlled by Ca 2ϩ (for review, see references [9,10]). Some experiments indicated that I K(Ca) was activated by an influx of Ca 2ϩ when the cell was superfused with hyposmotic solution [6,11,12]. Other experiments have shown that I K(Ca) is activated by an intracellular Ca 2ϩ signal that is released from intracellular calcium stores during RVD [13]. But the effect of hyposmotic swelling on I K(Ca) and the role of intracellular or extracellular Ca 2ϩ in gastric smooth muscle cells has not been investigated.In our previous study, we reported that the voltageoperated calcium current (I Ca ) was increased [14] and that the volume-sensitive chloride current (I Cl ) was activated by hyposmotic swelling [15] in gastric antral myocytes of the guinea-pig. In the present study, we Key words: gastric smooth muscle cell, Ca 2ϩ -activated K ϩ current, Ca 2ϩ -induced Ca 2ϩ release, swelling.Abstract: In our study of the effects of hyposmotic swelling on the Ca 2ϩ -activated potassium currents [I K(Ca) ] and its mechanism, we employed the whole-cell patch clamp technique using the gastric antral circular myocytes of the guinea-pig. Hyposmotic swelling efficiently increased I K(Ca) , and the extent of changes in I K(Ca) was sharply dependent on the osmolarity of the perfusion solutions. When the calcium-free solution (EGTA 10 M added in calcium-free solution) was superfused, I K(Ca) was not increased by the hyposmotic swelling. Gadolinium (Gd 3ϩ ) 100 nM, a blocker of the stretch-activated nonselective cation channel, blocked the activation of I K(Ca) induced by hyposmotic swelling, but nicardipine 5 M (the Ltype calcium channel blocker) did not. Heparin 3 mg/ml, a potent inhibitor of inositol triphosphate receptor (InsP 3 R), did not inhibit the response, and caffeine 1 mM (the agonist for calcium-induced calcium release [CICR]) imitated the effect of hyposmotic swelling. Ryanodine (15 M), markedly inhibited the effect. These results suggest that hyposmotic swelling activates I K(Ca) , and the activation is associated with CICR, which is triggered by extracellular calcium influx through the stretch-activated channel (SA channel).

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Interactions of sodium transport, cell volume, and calcium in frog urinary bladder.

Cited by 47 publications

References 34 publications

Ca2+ sensitivity of volume‐regulatory K+ and Cl‐ channels in cultured human epithelial cells.

Ca2+ sensitivity of volume‐regulatory K+ and Cl‐ channels in cultured human epithelial cells.

Cell Volume Regulation in Nonrenal Epithelia

The Involvement of Calcium Mobilization in the Calcium-Activated Potassium Currents Activated by Hyposmotic Swelling in Gastric Antral Circular Myocytes of the Guinea-Pig.

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