Calcium-activated potassium channels and their role in secretion

Petersen, O. H.; Maruyama, Yoshio

doi:10.1038/307693a0

Cited by 657 publications

(311 citation statements)

References 65 publications

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“…In view of this it is curious that isoprenaline failed to increase 86Rb efflux from guinea-pig trachealis. Airways smooth muscle may contain several kinds of K+ channel (Inoue et al, 1983) and the K+ channels of excitable cells may not all be permeable to 86Rb (Petersen & Maruyama, 1984). This raises the possibility that isoprenaline opens trachealis K+-channels which are impermeable to 86Rb.…”

Section: Resultsmentioning

confidence: 99%

The relaxant action of nicorandil in guinea‐pig isolated trachealis

Allen

Foster

Morgan

et al. 1986

British J Pharmacology

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Nicorandil (1–1000 μmol 1–1) caused concentration‐dependent relaxation of guinea‐pig isolated trachealis. Propranolol (1 μmol 1−1) did not modify the relaxant action of nicorandil but antagonized isoprenaline. Among K+‐channel inhibitors tested, apamin (0.1 μmol 1−1) and procaine (5 mmol 1−1) did not modify the relaxant action of nicorandil. In contrast, tetraethylammonium (TEA, 8 mmol 1−1) caused five fold antagonism. Trachealis exposed to K+‐rich (120 mmol 1−1) Krebs solution developed near‐maximal tension. Nicorandil relaxed the K+‐depolarized tissue though its concentration‐effect curve was shifted markedly to the right. In tissues in which tone was induced by histamine, methylene blue (100 μmol 1−1) antagonized nicorandil and sodium nitroprusside but did not modify the relaxant action of aminophylline. Intracellular electrophysiological recording showed that nicorandil (1 μmol 1−1) could evoke some relaxation in the absence of electrical changes. Higher concentrations (10–1000 μmol 1−1) reduced the amplitude and frequency of spontaneous electrical slow waves. Nicorandil also caused concentration‐dependent hyperpolarization and relaxation. When the hyperpolarization was sufficiently pronounced slow wave activity was abolished. TEA (8 mmol 1−1) induced slow waves which were surmounted by a spike potential. TEA slightly reduced the maximal hyperpolarization induced by nicorandil and increased the time required for nicorandil to abolish slow wave discharge. Procaine (5 mmol 1−1) induced slow waves of relatively low frequency. Sometimes these were surmounted by a spike potential. Procaine markedly reduced the hyperpolarization induced by nicorandil and increased the time required for abolition of slow waves. In studies of the efflux of 86Rb+ from muscle‐rich strips of trachea, nicorandil (1000 μmol 1−1) increased the efflux rate constant, whereas isoprenaline (1 μmol 1−1) was without effect. It is concluded that nicorandil‐induced relaxation does not involve the activation of β‐adrenoceptors but is partly attributable to the formation of nitric oxide from the nitrate moiety in its molecular structure. Nicorandil can evoke relaxation in the absence of membrane potential change but towards the upper end of its effective concentration range, nicorandil increases membrane K+ conductance and thereby evokes hyperpolarization of trachealis cells. The K+ channels opened by nicorandil are permeable to 86Rb, insensitive to apamin and TEA but may be inhibited by procaine.

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Section: Resultsmentioning

confidence: 99%

The relaxant action of nicorandil in guinea‐pig isolated trachealis

Allen

Foster

Morgan

et al. 1986

British J Pharmacology

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“…It is well documented that basolateral K ϩ channels, which can be blocked by Ba 2ϩ , make an important contribution to the maintenance of membrane potential (V m ) in epithelial cells (32), and such channels could thus play an important role in epithelial Na ϩ transport by maintaining the driving force for Na ϩ entry (25,27). The present study, in common with earlier data (27), showed clearly that Ba 2ϩ abolishes the response to isoprenaline, but, in our hands, this cation caused only transient inhibition of basal I sc .…”

Section: Discussionmentioning

confidence: 99%

β-Adrenoceptor-mediated control of apical membrane conductive properties in fetal distal lung epithelia

Collett

Ramminger

Olver

et al. 2002

American Journal of Physiology-Lung Cellular and Molecular Phys

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Distal lung epithelial cells isolated from fetal rats were cultured (48 h) on permeable supports so that transepithelial ion transport could be quantified electrometrically. Unstimulated cells generated a short-circuit current (Isc) that was inhibited (ϳ80%) by apical amiloride. The current is thus due, predominantly, to the absorption of Na ϩ from the apical solution. Isoprenaline increased the amiloride-sensitive Isc about twofold. Experiments in which apical membrane Na ϩ currents were monitored in basolaterally permeabilized cells showed that this was accompanied by a rise in apical Na ϩ conductance (GNaϩ). Isoprenaline also increased apical Cl Ϫ conductance (GClϪ) by activating an anion channel species sensitive to glibenclamide but unaffected by 4,4Ј-diisothiocyanatostilbene-2,2Ј-disulfonic acid (DIDS). The isoprenaline-evoked changes in G Na ϩ and GClϪ could account for the changes in Isc observed in intact cells. Glibenclamide had no effect upon the isoprenaline-evoked stimulation of I sc or GNaϩ demonstrating that the rise in GClϪ is not essential to the stimulation of Na ϩ transport. alveolar ion transport; Ussing chambers; permeabilized epithelia THROUGHOUT FETAL LIFE the distal lung epithelia secrete fluid into the developing air spaces (31) and establish a distending pressure that is crucial to lung morphogenesis (11). However, this liquid must be removed from the lungs if the newborn infant is to breathe at birth. The absorption of this liquid occurs during the final stages of gestation and is dependent upon the active withdrawal of Na ϩ from the lung lumen, a process that can be controlled via ␤-adrenoceptors (23,30,(36)(37)(38). The means by which this control is achieved are not fully understood, but there is evidence that the process involves a rise in apical Na ϩ conductance (G Na ϩ) (15,20). It is also known that ␤-adrenoceptor agonists can increase apical Cl Ϫ conductance (G Cl Ϫ) in these cells, and it has been suggested that this may facilitate Na ϩ transport by increasing the driving force for Na ϩ entry (16,29). It is, however, difficult to see how the ionic gradients that normally prevail in epithelial cells could allow Na ϩ transport to be controlled in this way (see Refs. 20,44). To clarify the means by which ␤-adrenoceptor agonists can control Na ϩ absorption in the distal lung epithelia, we now explore the effects of isoprenaline upon the conductive properties of the apical membrane. METHODS Isolation and culture of rat fetal distal lung epithelial cells.Fetuses removed from anesthetized (3% halothane), 20-day pregnant (term ϭ 22 days) rats were immediately decapitated, and their lung tissue was collected into ice-cold, Ca 2ϩ -and Mg 2ϩ -free Hanks' balanced salt solution. The anesthetized animals were then killed (cervical dislocation/exsanguination) before regaining consciousness. The fetal lung tissue was chopped into pieces (Ͻ0.5 mm) and disaggregated using 0.2% trypsin/0.012% DNase (2 ϫ 20 min, 37°C) followed by 0.1% collagenase/0.012% DNase [15 min, 37°C, both in Dulbecco's mo...

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“…Therefore, it would be interesting to relate actions of these sensory neuropeptides and chemical mediators to the modulation of K ‫ם‬ and Cl ‫מ‬ conductances in dental pulp cells. As described in a wide variety of cells, ion channels can be involved in the signal codes for proliferation, secretion of extracellular matrix proteins and cell differentiation 8,11,20,22) as well as the intercellular electrical/chemical communications through gap junctions 2,3,8,9,19,21,24,28) . The K ‫ם‬ and Cl ‫מ‬ channels expressed in dental pulp cells are most likely responsible for cellular functions underlying dental pulp metabolisms.…”

Section: Discussionmentioning

confidence: 99%

A small-conductance Ca2+-activated K+ current and Cl- current in rat dental pulp cells.

Shibukawa

Suzuki

2000

Bull. Tokyo Dent. Coll.

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We characterized a voltage-dependent ionic current in dental pulp cells on dental pulp slices using a nystatin perforated-patch recording configuration. The outward currents in dental pulp cells were inhibited by the following channel blockers: 1) Ca ‫ם2‬ -free extracellular solution containing 10mM Ba ‫ם2‬ , 2) extracellular 400 nM apamin and 3) extracellular 300 nM 4,4Ј-diisothiocyanatostilbene-2,2Ј-disulfonic acid (DIDS). On the other hand, 15mM tetraethylammonium (TEA) did not inhibit the outward currents. The inhibitory effects of Ca ‫ם2‬ -free extracellular solution, apamin and DIDS had voltagedependency. These results indicated that dental pulp cells expressed a small-conductance Ca ‫ם2‬ -activated K ‫ם‬ current (SK current) and a DIDS-sensitive Cl ‫מ‬ current. The functional significance of these channels is discussed.

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Calcium-activated potassium channels and their role in secretion

Abstract: Single-channel recording by the patch-clamp technique has now characterized three kinds of membrane potassium channels activated by intracellular calcium ions in animal cells. These play a crucial part in the regulation of membrane potential and of secretion.

Cited by 657 publications

References 65 publications

The relaxant action of nicorandil in guinea‐pig isolated trachealis

The relaxant action of nicorandil in guinea‐pig isolated trachealis

β-Adrenoceptor-mediated control of apical membrane conductive properties in fetal distal lung epithelia

A small-conductance Ca2+-activated K+ current and Cl- current in rat dental pulp cells.

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