Activation of basolateral Cl? channels in the rat colonic epithelium during regulatory volume decrease

Diener, Martin; Nobles, Muriel; Rummel, W.

doi:10.1007/bf00375048

Cited by 46 publications

(48 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Following a hypotonic stress the transepithelial resistance showed an increase during the swelling phase, followed by a slow recovery towards the initial value after 60·min exposure. These R te changes, similar to those observed for other intestinal epithelia such as rat colonic epithelium (Diener et al, 1992) and rat small intestine (Diener et al, 1996), are in the direction expected for narrowing of lateral intercellular spaces during the swelling phase, followed by their slow widening in the RVD phase. However, hypotonicity induced changes in junctional resistance cannot be ruled out.…”

Section: Discussionsupporting

confidence: 82%

See 1 more Smart Citation

Hypotonicity induced K+ and anion conductive pathways activation in eel intestinal epithelium

Lionetto

Giordano

Nuccio

et al. 2005

Journal of Experimental Biology

View full text Add to dashboard Cite

show abstract

Section: Discussionsupporting

confidence: 82%

“…In all the experiments the hypotonic stress applied was a 45% percentage decrease in osmolarity of the perfusion solution; this represents a commonly used hypotonic stress in volume regulation protocols (Hoffmann, 1978;Hazama and Okada, 1990;Diener et al, 1992).…”

Section: Rvd Response In Eel Intestinal Epitheliummentioning

confidence: 99%

Hypotonicity induced K+ and anion conductive pathways activation in eel intestinal epithelium

Lionetto

Giordano

Nuccio

et al. 2005

Journal of Experimental Biology

View full text Add to dashboard Cite

show abstract

“…Our whole-cell current data as well as the single channel current data from cell-attached patches therefore provide evidence for a cell swelling-induced coactivation of K+ and Cl-channels. A similar coactivation at the single channel level has also been demonstrated in MDCK cells (Banderali & Roy, 1992b;Roy & Banderali, 1994 (Diener et al 1992). …”

Section: Resultssupporting

confidence: 70%

“…Large currents developed in cells challenged with hypotonic extracellular solutions (HTSs). Figure 2A shows for Cl-channels (Diener, Nobles & Rummel, 1992;Ehrenfeld Raschi & Brochiero, 1994). The contributions of K+ and Cl-to the HTS-induced current might therefore be obtained from the difference in HTS-activated current measured in the presence and absence of these respective blockers.…”

Section: Resultsmentioning

confidence: 99%

Volume regulation in a toad epithelial cell line: role of coactivation of K+ and Cl‐ channels.

Nilius

Sehrer

Smet

et al. 1995

The Journal of Physiology

View full text Add to dashboard Cite

1. We have measured changes in cell volume, membrane potential and ionic currents in distal nephron A6 cells following a challenge with hypotonic solutions (HTS). 2. The volume increase induced by HTS is compensated by a regulatory volume decrease (RVD), which is inhibited by both 5-nitro-2-(3-phenylpropylamino)-benzoate (NPPB) and quinine. Quinine (500 uM) completely blocked RVD, whereas 100 /M NPPB delayed and attenuated RVD.3. The resting potential in A6 cells was -52-3 + 4.8 mV (n = 53), and shifted to -35-1 + 2-2 mV (n = 33) during HTS. 4. Resting membrane current in A6 cells was 0 35 + 0-12 pA pF-1 at -80 mV and 0-51 + 0-16 pA pF-1 at +80 mV (n = 5). During cell swelling these values increased to 11.5 + 1 1 and 29-3 + 2-8 pA pF-1 (n = 29), respectively. 5. Quinine (500 /zM) completely blocked the HTS-activated current at -15 mV, the reversal potential for Cl-currents, but exerted only a small block at -100 mV (K+ equilibrium potential). NPPB (100 /M) inhibited the current at both potentials almost to the same extent. The HTS-induced net current reversed at -41 + 2-5 mV (n = 15), which is close to the measured resting potential during HTS. 6. The quinine-insensitive current reversed near the Cl-equilibrium potential. The quininesensitive current reversed near the K+ equilibrium potential. The respective conductances activated by HTS at the zero-current potential were 2-1 + 0 7 nS for K+ and 5-2 + 1-3 nS for Cl (n = 15). 7. Single channel analysis unveiled activation of at least two different channels during HTS.A 36 pS channel reversing at the Cl-equilibrium potential showed increased open probability at depolarized potentials. HTS also activated a K+ channel with a 29 pS conductance in high-K+ extracellular solutions (130 mM) or 12 pS in 2-5 mm K+.8. This coactivation of K+ and Cl-channels shifts the membrane potential towards a value between EK and Eci (the reversal potentials for K+ and CF), where a net efflux of Cl-(Clinward current) and K+ (K+ outward current) under zero-current conditions occurs. Block of either the K+ or the Cl-conductance will shift the zero-current potential towards the equilibrium potential of the unblocked channel, preventing net efflux of osmolytes and RVD. This coactivation of K+ and Cl-currents causes a shift of osmolytes out of the cells, which almost completely accounts for the observed RVD.Processes involved in the regulation of cell volume have We have recently shown that a challenge with hyposmotic been widely studied during the last 10 years (for reviews, solutions was not followed by a regulatory volume decrease see McCarty

show abstract

“…Interestingly, either anion or cation channel blocker alone could inhibit both the swelling-induced cation and anion currents. It was also observed in previous studies in rat colonic epithelium (Diener, Nobles & Rummel, 1992) and human intestinal epithelial cells (Kubo & Okada, 1992) that an individual channel blocker could block RVD completely. However, there was a noticeable discrepancy between the results obtained from whole-cell patch-clamp studies and those from cell size measurements in that Ba2+ had no effect on the swelling-induced conductances in the former but blocked RVD in the latter.…”

Section: C1-dependence Of the Swelling-induced Cation Conductancementioning

confidence: 59%

Swelling‐induced anion and cation conductances in human epididymal cells.

Chan¹,

Fu²,

Chung³

et al. 1994

The Journal of Physiology

View full text Add to dashboard Cite

1. Activation of both anion and cation conductances was observed in primary cultured human epididymal cells during osmotic swelling under the patch-clamp whole-cell configuration. The swelling-induced anion conductance was 25-66 + 4 70 nS and the cation conductance was 7 35 + 1P40 nS. The permeability ratio of K+ to Cl-(PK/PC1) was calculated to be 0-40. Known anion or cation channel blockers could inhibit both conductances simultaneously. 2. When the major permeant ion species in the pipette and bath solution was Cl-, the mean conductance was found to be 17-06 + 1'8 nS, significantly smaller than that obtained in the presence of intracellular K', 25166 + 4 70 nS (P < 0 05). No significant current activation was observed when solutions containing only K+ as the permeant ion were used. 3. When the anionic amino acids glutamate and aspartate were used to replace extracellular Cl-, the permeability ratios were calculated to be PG1ut/IPcl = 020 and PASP/Pc1 = 0-17.4. The cation conductance was found to be non-selective since its permeability to other cations such as Na+ and choline, an organic compound highly concentrated in epididymal fluid, was similar to that of K+. 5. Regulatory volume decrease (RVD) was observed after initial osmotic swelling; this could be inhibited by either anion or cation channel blockers. 6. The results of this study suggest that both anion and cation conductances are activated during cellular swelling, and indicate the existence of an interdependent relationship between the swelling-induced cation and anion conductances. Both swelling-induced cation and anion conductances are involved in the volume regulatory process and may be responsible for transporting amino acids or organic compounds in human epididymal cells.

show abstract

Activation of basolateral Cl? channels in the rat colonic epithelium during regulatory volume decrease

Cited by 46 publications

References 33 publications

Hypotonicity induced K+ and anion conductive pathways activation in eel intestinal epithelium

Hypotonicity induced K+ and anion conductive pathways activation in eel intestinal epithelium

Volume regulation in a toad epithelial cell line: role of coactivation of K+ and Cl‐ channels.

Swelling‐induced anion and cation conductances in human epididymal cells.

Contact Info

Product

Resources

About