An Anion Channel in Guinea Pig Gallbladder Epithelial Cells Is Highly Permeable to HCO−3

Meyer, Gerd; Garavaglia, Maria Lisa; Bazzini, Claudia; Botta, Guido Fernando

doi:10.1006/bbrc.2000.3400

Cited by 13 publications

(14 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This contention is substantiated by the observation that duodenal epithelial cells obtained from patients with cystic fibrosis (CF) have impaired pH i recovery from alkaline loads in chloride-free medium (50). Furthermore, our results are also consistent with the presence of a CFTRlike, NPPB-sensitive bicarbonate-selective anion channel in the apical membrane, as has been described recently for guinea pig gallbladder (51).…”

Section: Figuresupporting

confidence: 90%

Cellular bicarbonate protects rat duodenal mucosa from acid-induced injury

Akiba¹,

Furukawa²,

Guth³

et al. 2001

J. Clin. Invest.

View full text Add to dashboard Cite

Section: Figuresupporting

confidence: 90%

Cellular bicarbonate protects rat duodenal mucosa from acid-induced injury

Akiba¹,

Furukawa²,

Guth³

et al. 2001

J. Clin. Invest.

View full text Add to dashboard Cite

“…Patch-clamp experiments were performed as previously reported (32). The patch pipette resistance was 5-10 M⍀, and seal resistance was 5-10 G⍀.…”

Section: Methodsmentioning

confidence: 99%

Upregulation of apical sodium-chloride cotransporter and basolateral chloride channels is responsible for the maintenance of salt-sensitive hypertension

Capasso¹,

Rizzo

Garavaglia

et al. 2008

American Journal of Physiology-Renal Physiology

Self Cite

View full text Add to dashboard Cite

. Upregulation of apical sodium-chloride cotransporter and basolateral chloride channels is responsible for the maintenance of salt-sensitive hypertension. Am J Physiol Renal Physiol 295: F556 -F567, 2008. First published May 14, 2008 doi:10.1152/ajprenal.00340.2007.-We investigated which of the NaCl transporters are involved in the maintenance of salt-sensitive hypertension. Milan hypertensive (MHS) rats were studied 3 mo after birth. In MHS, compared with normotensive strain (MNS), mRNA abundance, quantified by competitive PCR on isolated tubules, was unchanged, both for Na ϩ /H ϩ isoform 3 (NHE3) and Na. These results were confirmed by Western blots, which revealed: 1) unchanged NHE3 in the cortex and NKCC2 in the outer medulla; 2) a significant increase (52%, n ϭ 6, P Ͻ 0.001) of NCC in the cortex; 3) ␣-and ␤-sodium channels [epithelial Na ϩ channel (ENaC)] unaffected in renal cortex and slightly reduced in the outer medulla, while ␥-ENaC remained unchanged. Pendrin protein expression was unaffected. The role of NCC was reinforced by immunocytochemical studies showing increased NCC on the apical membrane of DCT cells of MHS animals, and by clearance experiments demonstrating a larger sensitivity (P Ͻ 0.001) to bendroflumethiazide in MHS rats. Kidneyspecific chloride channels (ClC-K) were studied by Western blot experiments on renal cortex and by patch-clamp studies on primary culture of DCT dissected from MNS and MHS animals. Electrophysiological characteristics of ClC-K channels were unchanged in MHS rats, but the number of active channels in a patch was 0.60 Ϯ 0.21 (n ϭ 35) in MNS rats and 2.17 Ϯ 0.59 (n ϭ 23) in MHS rats (P Ͻ 0.05). The data indicate that, in salt-sensitive hypertension, there is a strong upregulation, both of NCC and ClC-K along the DCT, which explains the persistence of hypertension. type 3 sodium/hydrogen exchanger; sodium-potassium 2 chloride cotransporter; sodium-chloride cotransporter; epithelial sodium channel; kidney-specific chloride channel; pendrin; aldosterone HYPERTENSION IS THE MOST IMPORTANT risk factor for diseases of several organs, including heart, brain, and kidney. Despite the impressive number of studies, the etiology of hypertension is still incompletely understood. However,

show abstract

“…The patch-clamp technique and the corresponding statistics were applied as reported (26,27). In the whole-cell configuration, the resistances of the microelectrodes and of the seals were 2-8 m⍀ and 1-2 G⍀, respectively.…”

Section: Patch-clamp Techniquementioning

confidence: 99%

Hypotonicity Induces Aquaporin-2 Internalization and Cytosol-to-Membrane Translocation of ICln in Renal Cells

et al. 2007

Self Cite

View full text Add to dashboard Cite

Kidney collecting-duct cells swell in response to changes in medulla osmolality caused by the transition from antidiuresis to diuresis. Regulatory volume decrease (RVD) mechanisms must be activated to face this hypotonic stress. In Aquaporin-2 (AQP2)-expressing renal CD8 cells, hypotonicity decreased cell surface expression of AQP2 and increased the amount of AQP2 localized intracellularly, whereas the total amount of AQP2 phosphorylated at ser-256 decreased. Analysis of cAMP dynamics using fluorescence resonance energy transfer (FRET) showed that hypotonicity causes a reduction of cAMP, consistent with a decrease in phospho-AQP2. Moreover, hypotonicity caused a profound actin reorganization, associated with the loss of stress fibers and formation of F-actin patches (microspikes) at the cell border. Those changes were regulated by the monomeric GTPase Cdc42. Interestingly, expression of the dominant-negative Cdc42 (N17-Cdc42) prevented the hypotonicity-induced microspike formation and the generation of Cl(-) currents. Hypotonicity also caused the relocation from the cytosol to the plasma membrane and increase in interaction with actin of ICln (nucleotide-sensitive chloride current protein), which is essential for the generation of ion currents activated during RVD. Together, the profound actin remodeling, internalization of AQP2 and translocation of ICln to the plasma membrane during hypotonicity may contribute to RVD after cell swelling in renal medulla.

show abstract

An Anion Channel in Guinea Pig Gallbladder Epithelial Cells Is Highly Permeable to HCO−3

Cited by 13 publications

References 43 publications

Cellular bicarbonate protects rat duodenal mucosa from acid-induced injury

Cellular bicarbonate protects rat duodenal mucosa from acid-induced injury

Upregulation of apical sodium-chloride cotransporter and basolateral chloride channels is responsible for the maintenance of salt-sensitive hypertension

Hypotonicity Induces Aquaporin-2 Internalization and Cytosol-to-Membrane Translocation of ICln in Renal Cells

Contact Info

Product

Resources

About