Chloride channels of high conductance in the microvillous membrane of term human placenta

Brown, Peter de Nully; Greenwood, Susan; Robinson, J.; Boyd, Robert D.

doi:10.1016/s0143-4004(05)80253-x

Cited by 45 publications

(31 citation statements)

References 21 publications

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“…These channels were similar to those observed in cultured cortical astrocytes from rats [4,49,50] and mice [5][6][7]51] as well as in a rat astrocytic RGCN cell line [52]. In epithelia, the urinary bladder [53], gastric [54], pancreatic [55][56][57], colonic [58][59][60], airway [61][62][63], choroid plexus [64], bile duct [65,66], ciliary [67][68][69], renal [9,19,[70][71][72][73][74][75][76][77][78], vestibular [79], placental [80][81][82][83][84][85][86], ruminal [87] and ovarian [84] epithelial cells were also found to express the maxianion channel with properties similar to those of excitable cells. Resembling maxi-anion channels were also found in fibroblasts [14,…”

Section: Expression Pattern Of the Maxi-anion Channelsupporting

confidence: 80%

The maxi-anion channel: a classical channel playing novel roles through an unidentified molecular entity

Sabirov

Okada

2008

J Physiol Sci

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The maxi-anion channel is widely expressed and found in almost every part of the body. The channel is activated in response to osmotic cell swelling, to excision of the membrane patch, and also to some other physiologically and pathophysiologically relevant stimuli, such as salt stress in kidney macula densa as well as ischemia/ hypoxia in heart and brain. Biophysically, the maxi-anion channel is characterized by a large single-channel conductance of 300-400 pS, which saturates at 580-640 pS with increasing the Cl -concentration. The channel discriminates well between Na ? and Cl -, but is poorly selective to other halides exhibiting weak electric-field selectivity with an Eisenman's selectivity sequence I. The maxi-anion channel has a wide pore with an effective radius of *1.3 nm and permits passage not only of Cl -but also of some intracellular large organic anions, thereby releasing major extracellular signals and gliotransmitters such as glutamate -and ATP 4-. The channel-mediated efflux of these signaling molecules is associated with kidney tubuloglomerular feedback, cardiac ischemia/hypoxia, as well as brain ischemia/hypoxia and excitotoxic neurodegeneration. Despite the ubiquitous expression, well-defined properties and physiological/pathophysiological significance of this classical channel, the molecular entity has not been identified. Molecular identification of the maxi-anion channel is an urgent task that would greatly promote investigation in the fields not only of anion channel but also of physiological/pathophysiological signaling in the brain, heart and kidney.

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Section: Expression Pattern Of the Maxi-anion Channelsupporting

confidence: 80%

The maxi-anion channel: a classical channel playing novel roles through an unidentified molecular entity

Sabirov

Okada

2008

J Physiol Sci

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“…In addition, maxi-Cl channels (Fig. 14), with similar properties to those observed in a range of human tissues (36,110,156), are found in apical membrane patches (172). These channels are DIDS sensitive, with a large unit conductance of 280 pS (172).…”

Section: B Patch Clamp Reveals Maxi-chloride Channels In Tubulessupporting

confidence: 57%

“…These channels are DIDS sensitive, with a large unit conductance of 280 pS (172). Consistent with the action of leucokinin to raise calcium, vertebrate maxi-Cl channels are known to be Ca 2ϩ sensitive (36,110,156).…”

Section: B Patch Clamp Reveals Maxi-chloride Channels In Tubulesmentioning

confidence: 95%

Integrative Physiology and Functional Genomics of Epithelial Function in a Genetic Model Organism

Dow

Davies

2003

Physiological Reviews

115

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Dow, Julian A. T, and Shireen A. Davies. Integrative Physiology and Functional Genomics of Epithelial Function in a Genetic Model Organism. Physiol Rev 83: 687–729, 2003; 10.1152/physrev.00035.2002.—Classically, biologists try to understand their complex systems by simplifying them to a level where the problem is tractable, typically moving from whole animal and organ-level biology to the immensely powerful “cellular” and “molecular” approaches. However, the limitations of this reductionist approach are becoming apparent, leading to calls for a new, “integrative” physiology. Rather than use the term as a rallying cry for classical organismal physiology, we have defined it as the study of how gene products integrate into the function of whole tissues and intact organisms. From this viewpoint, the convergence between integrative physiology and functional genomics becomes clear; both seek to understand gene function in an organismal context, and both draw heavily on transgenics and genetics in genetic models to achieve their goal. This convergence between historically divergent fields provides powerful leverage to those physiologists who can phrase their research questions in a particular way. In particular, the use of appropriate genetic model organisms provides a wealth of technologies (of which microarrays and knock-outs are but two) that allow a new precision in physiological analysis. We illustrate this approach with an epithelial model system, the Malpighian (renal) tubule of Drosophila melanogaster. With the use of the beautiful genetic tools and extensive genomic resources characteristic of this genetic model, it has been possible to gain unique insights into the structure, function, and control of epithelia.

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“…Previous autoradiographic studies (Koseki et al 1989) and endothelin binding studies (Takahashi et al 1990) (Klockner & Isenberg, 1991;Van Renterghem & Lazdunski, 1993) and to inhibit cyclic AMP-activated Cl-channels in cardiac ventricular myocytes (James, Xie, Fujitani, Hayashi & Horie, 1994 Ca2+-dependent ); (2) PTX-sensitive G protein-regulated (Schwiebert, Light, Fejes-Toth, NarayFejes-Toth & Stanton, 1990;McGill, Gettys, Basavappa & Fitz, 1993); (3) SITS-or DIDS-sensitive (Nelson, Tang & Palmer, 1984;Hanrahan, Alles & Lewis, 1985;Kolb, Brown & Murer, 1985;Schneider, Cook, Gage & Young, 1985;Velasco, Prieto, Alvarez-Riera, Gascon & Barros, 1989;Light et al 1990;Becq, Fanjul, Mahieu, Berger, Gola & Hollande, 1992;Brown, Greenwood, Robinson & Boyd, 1993); and (4) voltage-activated Cl-channels with a bellshaped voltage dependency McGill, Basavappa & Fitz, 1992;Brown et al 1993 Both the ETB receptors and the coupled Cl-channels appear to reside on the basolateral membrane but not on the luminal membrane, because the time courses of Clcurrent activation by (basolateral) addition of ET-1, of the current profile changes in response to reduction of the (basolateral) Cl-concentration, and of Cl-current inhibition by (basolateral) addition of NPPB were not different between parietal cells singly isolated and those within gastric glands, the luminal membrane of which is not readily exposed to the basolateral bathing solution.…”

Section: Discussionmentioning

confidence: 99%

A maxi Cl‐ channel coupled to endothelin B receptors in the basolateral membrane of guinea‐pig parietal cells.

Kajita

Kotera

Shirakata

et al. 1995

The Journal of Physiology

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1. To study endothelin (ET) receptors in guinea-pig stomach, ET-binding assays and in vitro autoradiography were performed on fundic cell suspensions and on sections of the fundus, respectively. ETA and ETB receptor subtypes were found to coexist in the parietal cells. 2. Endothelin 1 (ET-1) added to the (basolateral) bathing solution was found to activate noisy whole-cell Cl-currents within about 1 min in both single, isolated parietal cells and those within gastric glands obtained from the fundus. 3. ET-1-induced Cl-currents were rapidly blocked by a Cl-channel blocker (NPPB) added to the (basolateral) bathing solution in a concentration-dependent manner with a halfmaximum inhibition concentration of 33/uM. 4. The anion selectivity sequence of the ET-1-induced conductance was I > Br-> Cl-> F-, corresponding to Eisenmans sequence I.5. Changes in extracellular pH between 5 and 8 did not affect the ET-1-induced activation of Cl currents. 6. Similar activating effects were also observed with ET-3 and a specific ETB receptor agonist (IRL1620). An ETB receptor antagonist (IRL1720) prevented the ET-1 effect, whereas an ETA-selective antagonist (FR139317 or BQ123) failed to antagonize the ET-1 effect. 7. In the whole-cell mode, unitary Cl-channel events could be observed in association with ET-1-activated macroscopic currents. The single-channel conductances were around 200 and 350 pS at negative and positive membrane potentials, respectively. 8. It is concluded that gastric parietal cells of guinea-pig possess pH-insensitive 'maxi' Clchannels coupled to ETB receptors in the basolateral membrane.

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Chloride channels of high conductance in the microvillous membrane of term human placenta

Cited by 45 publications

References 21 publications

The maxi-anion channel: a classical channel playing novel roles through an unidentified molecular entity

The maxi-anion channel: a classical channel playing novel roles through an unidentified molecular entity

Integrative Physiology and Functional Genomics of Epithelial Function in a Genetic Model Organism

A maxi Cl‐ channel coupled to endothelin B receptors in the basolateral membrane of guinea‐pig parietal cells.

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