Ca(2+)‐activated K+ channels modulate muscarinic secretion in cat chromaffin cells.

Uceda, G.; Artalejo, Antonio R.; López, Manuela G.; Abad, Francisco; Neher, Erwin; Garcı́a, Antonio G.

doi:10.1113/jphysiol.1992.sp019261

Cited by 48 publications

(29 citation statements)

References 38 publications

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“…Therefore, the activation of K~channels by elevated~Ca2~]would counteract the actions elicited by membrane depolarization and lead to a limit of further excitation (Tse and Hille, 1992). In fact, Ca2t dependent K~channel blockers have been reported to potentiate secretory responses to transmural electrical stimulation (Montiel et al, 1995) and to muscarinic stimulation (Uceda et al, 1992(Uceda et al, , 1994 in perfused cat adrenal glands. To define the physiological significance of Ca2tdependent K~channels in detail, further experiments must be performed, measuring simultaneously the secretory and current responses at a singlecell level.…”

Section: Discussionmentioning

confidence: 99%

Ca²⁺‐Dependent K⁺ Currents Induced by Muscarinic Receptor Activation in Guinea Pig Adrenal Chromaffin Cells

Ohta

Nakazato

1998

Journal of Neurochemistry

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Abstract:The characteristics of the outward current (/out) induced by muscarine were examined by using the whole-cell patch-clamp technique with a K~-containing pipette solution in combination with fura-2 microfluorometry in guinea pig chromaffin cells. Muscarine caused a transient increase in the cytosolic Ca2~concentration ([Ca2~])and activated an 'out with a reversal potential close to a Kẽquilibrium potential. Under symmetric K conditions, muscarine produced a transient inward current and an increase in [Ca2~]ãt -60 mV. At -15 mV, apamin and charybdotoxin, respective SK and BK channel blockers, decreased the 'out but scarcely affected the [Ca2~]response to muscarine. Muscarine produced an 1m~and an increase in [Ca2~]ẽven after a removal of external Ca2ã nd in the presence of 002+, indicating that these responses are mediated by Ca2~release from intracellular stores. The 'out evoked by the Ca2~release was much smaller than that evoked by the voltage-dependent Ca2ĩ nflux, even when similar [Ca2~]changes assessed by fura-2 microfluorometry occurred. Inositol 1 ,4,5-trisphosphate (lnsP 3) applied intracellularly and the photolysis of caged lnsP3 each evoked current changes similar to those induced by muscarine. These results indicate that the 'out evoked by muscarinic stimulation is mediated by Ca 2~-dependent Kchannels (probably BK and SK channels), which are activated by Ca2~released from intracellular Ca2~stores in guinea pig chromaffin cells.

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Section: Discussionmentioning

confidence: 99%

Ca²⁺‐Dependent K⁺ Currents Induced by Muscarinic Receptor Activation in Guinea Pig Adrenal Chromaffin Cells

Ohta

Nakazato

1998

Journal of Neurochemistry

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“…Although SK channels have been extensively characterized in neurons (16,24,25), where they mediate the afterhyperpolarization, and in some endocrine cells (26)(27)(28), where they are thought to regulate hormone secretion, the functions of ionic fluxes in nonexcitable cells, particularly immune cells (29,30), are only beginning to emerge. The specialized functions of neutrophils require that they release large quantities of ROS, proteases, and basic antimicrobial peptides.…”

Section: Discussionmentioning

confidence: 99%

SK channels mediate NADPH oxidase-independent reactive oxygen species production and apoptosis in granulocytes

Fay

Xiang²,

Jan³

2006

Proc. Natl. Acad. Sci. U.S.A.

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Neutrophils are immune cells that bind to, engulf, and destroy bacterial and fungal pathogens in infected tissue, and their clearance by apoptosis is essential for the resolution of inflammation. Killing involves both oxidative and nonoxidative processes, the oxidative pathway requiring electrogenic production of superoxide by the membrane-bound NADPH oxidase complex. A variety of stimuli, from bacterial chemotactic peptides to complement-or IgG-opsonized microbes, can induce the production of reactive oxygen species (ROS) by neutrophils, presumably by means of NADPH oxidase. We report here that 1-ethyl-2-benzimidazolinone (1-EBIO), an activator of Ca 2؉ -activated potassium channels of small conductance (SK) and intermediate conductance (IK), causes production of superoxide and hydrogen peroxide by neutrophils and granulocyte-differentiated PLB-985 cells. This response can be partially inhibited by the SK blocker apamin, which inhibits a Ca 2؉ -activated K ؉ current in these cells. Analysis of RNA transcripts indicates that channels encoded by the SK3 gene carry this current. The effects of 1-EBIO and apamin are independent of the NADPH oxidase pathway, as demonstrated by using a PLB-985 cell line lacking the gp91phox subunit. Rather, 1-EBIO and apamin modulate mitochondrial ROS production. Consistent with the enhanced ROS production and K ؉ efflux mediated by 1-EBIO, we found that this SK opener increased apoptosis of PLB-985 cells. Together, these findings suggest a previously uncharacterized mechanism for the regulation of neutrophil ROS production and programmed cell death.N eutrophils, as key players in the innate immune response, must be able to identify, phagocytose, and neutralize a broad array of pathogenic microbes (1). Killing usually involves isolation of bacteria or fungi within the phagosome, although neutrophils can release toxic contents into their surroundings to kill extracellular microbes (1). These toxic contents include reactive oxygen species (ROS), such as hydrogen peroxide and hypochlorous acid, as well as proteases and antimicrobial peptides. Because these toxins also can damage host cells, limiting their release and clearing apoptotic neutrophils ultimately are necessary for resolving an infection (2). Understanding how neutrophils regulate the production of oxidants is, therefore, important for both resisting pathogens and controlling inflammation.Although ion channels are best known for their roles in neuronal and cardiac action potentials, their importance in some immune cells, particularly neutrophils, has begun to emerge over the past few years (1, 3-5). The NADPH oxidase of neutrophils produces large amounts of superoxide at the plasma and phagosomal membranes, resulting in an electrogenic efflux of electrons from the cytoplasm (6). An extensive literature indicates that a proton channel, whose molecular identity has recently been identified (7,8), carries a compensating outward current that prevents depolarization of the cell membrane to potentials that inhibit the NADPH oxidase...

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“…In this line is the finding that muscarine produces a [Ca 2+ ] c elevation and an outward K + current, due to activation of Ca 2+ -activated K + channels in guinea-pig chromaffin cells [89]. These channels are regulating the nicotinic and muscarinic secretory response of cat and bovine chromaffin cells [90][91][92]. While ER Ca 2+ release by histamine causes a mild and transient catecholamine release response [93], a more sustained application causes a longer effect [93][94][95].…”

Section: Endoplasmic Reticulummentioning

confidence: 68%

Cytosolic organelles shape calcium signals and exo–endocytotic responses of chromaffin cells

et al. 2012

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a b s t r a c tfluxes between the different cell compartments support the proposal that the chromaffin cell has developed functional calcium tetrads formed by calcium channels, cytosolic calcium buffers, the endoplasmic reticulum, and mitochondria nearby the exocytotic plasmalemmal sites. These tetrads shape the Ca 2+ transients occurring during cell activation to regulate early and late steps of exocytosis, and the ensuing endocytotic responses. The different patterns of catecholamine secretion in response to stress may thus depend on such local [Ca 2+ ] c transients occurring at different cell compartments, and generated by redistribution and release of Ca 2+ by cytoplasmic organelles. In this manner, the calcium tetrads serve to couple the variable energy demands due to exo-endocytotic activities with energy production and protein synthesis.

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Ca(2+)‐activated K+ channels modulate muscarinic secretion in cat chromaffin cells.

Cited by 48 publications

References 38 publications

Ca²⁺‐Dependent K⁺ Currents Induced by Muscarinic Receptor Activation in Guinea Pig Adrenal Chromaffin Cells

Ca²⁺‐Dependent K⁺ Currents Induced by Muscarinic Receptor Activation in Guinea Pig Adrenal Chromaffin Cells

SK channels mediate NADPH oxidase-independent reactive oxygen species production and apoptosis in granulocytes

Cytosolic organelles shape calcium signals and exo–endocytotic responses of chromaffin cells

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Ca(2+)‐activated K+ channels modulate muscarinic secretion in cat chromaffin cells.

Cited by 48 publications

References 38 publications

Ca2+‐Dependent K+ Currents Induced by Muscarinic Receptor Activation in Guinea Pig Adrenal Chromaffin Cells

Ca2+‐Dependent K+ Currents Induced by Muscarinic Receptor Activation in Guinea Pig Adrenal Chromaffin Cells

SK channels mediate NADPH oxidase-independent reactive oxygen species production and apoptosis in granulocytes

Cytosolic organelles shape calcium signals and exo–endocytotic responses of chromaffin cells

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Ca²⁺‐Dependent K⁺ Currents Induced by Muscarinic Receptor Activation in Guinea Pig Adrenal Chromaffin Cells

Ca²⁺‐Dependent K⁺ Currents Induced by Muscarinic Receptor Activation in Guinea Pig Adrenal Chromaffin Cells