ChloroquineV1, PubMed, Curation, bibRecord, 000261

Involvement of large-conductance Ca2+-activated K+ channels in chloroquine-induced force alterations in pre-contracted airway smooth muscle.

Identifieur interne : 000261 ( PubMed/Curation ); précédent : 000260; suivant : 000262

Involvement of large-conductance Ca2+-activated K+ channels in chloroquine-induced force alterations in pre-contracted airway smooth muscle.

Source :

PloS one [ 1932-6203 ] ; 2015.

RBID : pubmed:25822280

Descripteurs français

English descriptors

KwdEn :
- Animals, Calcium Channel Blockers (pharmacology), Calcium Signaling (drug effects), Chloroquine (pharmacology), In Vitro Techniques, Large-Conductance Calcium-Activated Potassium Channels (antagonists & inhibitors), Large-Conductance Calcium-Activated Potassium Channels (physiology), Male, Mice, Mice, Inbred BALB C, Muscle Contraction (drug effects), Muscle Contraction (physiology), Muscle, Smooth (drug effects), Muscle, Smooth (physiology), Myocytes, Smooth Muscle (drug effects), Myocytes, Smooth Muscle (physiology), Patch-Clamp Techniques, Peptides (pharmacology), Ryanodine Receptor Calcium Release Channel (physiology), Trachea (cytology), Trachea (physiology).
MESH :
- chemical , antagonists & inhibitors : Large-Conductance Calcium-Activated Potassium Channels.
- chemical , pharmacology : Calcium Channel Blockers, Chloroquine, Peptides.
- cytology : Trachea.
- drug effects : Calcium Signaling, Muscle Contraction, Muscle, Smooth, Myocytes, Smooth Muscle.
- chemical , physiology : Large-Conductance Calcium-Activated Potassium Channels, Muscle Contraction, Muscle, Smooth, Myocytes, Smooth Muscle, Ryanodine Receptor Calcium Release Channel, Trachea.
- Animals, In Vitro Techniques, Male, Mice, Mice, Inbred BALB C, Patch-Clamp Techniques.

Abstract

The participation of large-conductance Ca2+ activated K+ channels (BKs) in chloroquine (chloro)-induced relaxation of precontracted airway smooth muscle (ASM) is currently undefined. In this study we found that iberiotoxin (IbTx, a selective inhibitor of BKs) and chloro both completely blocked spontaneous transient outward currents (STOCs) in single mouse tracheal smooth muscle cells, which suggests that chloro might block BKs. We further found that chloro inhibited Ca2+ sparks and caffeine-induced global Ca2+ increases. Moreover, chloro can directly block single BK currents completely from the intracellular side and partially from the extracellular side. All these data indicate that the chloro-induced inhibition of STOCs is due to the blockade of chloro on both BKs and ryanodine receptors (RyRs). We also found that low concentrations of chloro resulted in additional contractions in tracheal rings that were precontracted by acetylcholine (ACH). Increases in chloro concentration reversed the contractile actions to relaxations. In the presence of IbTx or paxilline (pax), BK blockers, chloro-induced contractions were inhibited, although the high concentrations of chloro-induced relaxations were not affected. Taken together, our results indicate that chloro blocks BKs and RyRs, resulting in abolishment of STOCs and occurrence of contraction, the latter will counteract the relaxations induced by high concentrations of chloro.

DOI: 10.1371/journal.pone.0121566
PubMed: 25822280

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<author><name sortKey="Qin, Gangjian" sort="Qin, Gangjian" uniqKey="Qin G" first="Gangjian" last="Qin">Gangjian Qin</name>
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<author><name sortKey="Zheng, Yun Min" sort="Zheng, Yun Min" uniqKey="Zheng Y" first="Yun-Min" last="Zheng">Yun-Min Zheng</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">Involvement of large-conductance Ca2+-activated K+ channels in chloroquine-induced force alterations in pre-contracted airway smooth muscle.</title>
<author><name sortKey="Wei, Ming Yu" sort="Wei, Ming Yu" uniqKey="Wei M" first="Ming-Yu" last="Wei">Ming-Yu Wei</name>
<affiliation wicri:level="1"><nlm:affiliation>Institute for Medical Biology & Hubei Provincial Key Laboratory for Protection and Application of Special Plants in Wuling Area of China, College of Life Sciences, South-Central University for Nationalities, Wuhan 430074, China.</nlm:affiliation>
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<author><name sortKey="Xue, Lu" sort="Xue, Lu" uniqKey="Xue L" first="Lu" last="Xue">Lu Xue</name>
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<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Institute for Medical Biology & Hubei Provincial Key Laboratory for Protection and Application of Special Plants in Wuling Area of China, College of Life Sciences, South-Central University for Nationalities, Wuhan 430074</wicri:regionArea>
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<author><name sortKey="Tan, Li" sort="Tan, Li" uniqKey="Tan L" first="Li" last="Tan">Li Tan</name>
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<author><name sortKey="Sai, Wen Bo" sort="Sai, Wen Bo" uniqKey="Sai W" first="Wen-Bo" last="Sai">Wen-Bo Sai</name>
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<author><name sortKey="Liu, Xiao Cao" sort="Liu, Xiao Cao" uniqKey="Liu X" first="Xiao-Cao" last="Liu">Xiao-Cao Liu</name>
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<country xml:lang="fr">République populaire de Chine</country>
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<author><name sortKey="Jiang, Qiu Ju" sort="Jiang, Qiu Ju" uniqKey="Jiang Q" first="Qiu-Ju" last="Jiang">Qiu-Ju Jiang</name>
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<author><name sortKey="Shen, Jinhua" sort="Shen, Jinhua" uniqKey="Shen J" first="Jinhua" last="Shen">Jinhua Shen</name>
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<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Institute for Medical Biology & Hubei Provincial Key Laboratory for Protection and Application of Special Plants in Wuling Area of China, College of Life Sciences, South-Central University for Nationalities, Wuhan 430074</wicri:regionArea>
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<author><name sortKey="Peng, Yong Bo" sort="Peng, Yong Bo" uniqKey="Peng Y" first="Yong-Bo" last="Peng">Yong-Bo Peng</name>
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<author><name sortKey="Zhao, Ping" sort="Zhao, Ping" uniqKey="Zhao P" first="Ping" last="Zhao">Ping Zhao</name>
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<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Institute for Medical Biology & Hubei Provincial Key Laboratory for Protection and Application of Special Plants in Wuling Area of China, College of Life Sciences, South-Central University for Nationalities, Wuhan 430074</wicri:regionArea>
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<author><name sortKey="Yu, Meng Fei" sort="Yu, Meng Fei" uniqKey="Yu M" first="Meng-Fei" last="Yu">Meng-Fei Yu</name>
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<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Institute for Medical Biology & Hubei Provincial Key Laboratory for Protection and Application of Special Plants in Wuling Area of China, College of Life Sciences, South-Central University for Nationalities, Wuhan 430074</wicri:regionArea>
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<author><name sortKey="Chen, Weiwei" sort="Chen, Weiwei" uniqKey="Chen W" first="Weiwei" last="Chen">Weiwei Chen</name>
<affiliation wicri:level="1"><nlm:affiliation>Institute for Medical Biology & Hubei Provincial Key Laboratory for Protection and Application of Special Plants in Wuling Area of China, College of Life Sciences, South-Central University for Nationalities, Wuhan 430074, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Institute for Medical Biology & Hubei Provincial Key Laboratory for Protection and Application of Special Plants in Wuling Area of China, College of Life Sciences, South-Central University for Nationalities, Wuhan 430074</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Ma, Li Qun" sort="Ma, Li Qun" uniqKey="Ma L" first="Li-Qun" last="Ma">Li-Qun Ma</name>
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<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Institute for Medical Biology & Hubei Provincial Key Laboratory for Protection and Application of Special Plants in Wuling Area of China, College of Life Sciences, South-Central University for Nationalities, Wuhan 430074</wicri:regionArea>
</affiliation>
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<author><name sortKey="Zhai, Kui" sort="Zhai, Kui" uniqKey="Zhai K" first="Kui" last="Zhai">Kui Zhai</name>
<affiliation wicri:level="1"><nlm:affiliation>National Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>National Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Zou, Chunbin" sort="Zou, Chunbin" uniqKey="Zou C" first="Chunbin" last="Zou">Chunbin Zou</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Medicine, Acute Lung Injury Center of Excellence, University of Pittsburgh, Pittsburgh, PA 15213, United States of America.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Medicine, Acute Lung Injury Center of Excellence, University of Pittsburgh, Pittsburgh, PA 15213</wicri:regionArea>
</affiliation>
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<author><name sortKey="Guo, Donglin" sort="Guo, Donglin" uniqKey="Guo D" first="Donglin" last="Guo">Donglin Guo</name>
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<front><div type="abstract" xml:lang="en">The participation of large-conductance Ca2+ activated K+ channels (BKs) in chloroquine (chloro)-induced relaxation of precontracted airway smooth muscle (ASM) is currently undefined. In this study we found that iberiotoxin (IbTx, a selective inhibitor of BKs) and chloro both completely blocked spontaneous transient outward currents (STOCs) in single mouse tracheal smooth muscle cells, which suggests that chloro might block BKs. We further found that chloro inhibited Ca2+ sparks and caffeine-induced global Ca2+ increases. Moreover, chloro can directly block single BK currents completely from the intracellular side and partially from the extracellular side. All these data indicate that the chloro-induced inhibition of STOCs is due to the blockade of chloro on both BKs and ryanodine receptors (RyRs). We also found that low concentrations of chloro resulted in additional contractions in tracheal rings that were precontracted by acetylcholine (ACH). Increases in chloro concentration reversed the contractile actions to relaxations. In the presence of IbTx or paxilline (pax), BK blockers, chloro-induced contractions were inhibited, although the high concentrations of chloro-induced relaxations were not affected. Taken together, our results indicate that chloro blocks BKs and RyRs, resulting in abolishment of STOCs and occurrence of contraction, the latter will counteract the relaxations induced by high concentrations of chloro. </div>
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<ArticleTitle>Involvement of large-conductance Ca2+-activated K+ channels in chloroquine-induced force alterations in pre-contracted airway smooth muscle.</ArticleTitle>
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<Abstract><AbstractText>The participation of large-conductance Ca2+ activated K+ channels (BKs) in chloroquine (chloro)-induced relaxation of precontracted airway smooth muscle (ASM) is currently undefined. In this study we found that iberiotoxin (IbTx, a selective inhibitor of BKs) and chloro both completely blocked spontaneous transient outward currents (STOCs) in single mouse tracheal smooth muscle cells, which suggests that chloro might block BKs. We further found that chloro inhibited Ca2+ sparks and caffeine-induced global Ca2+ increases. Moreover, chloro can directly block single BK currents completely from the intracellular side and partially from the extracellular side. All these data indicate that the chloro-induced inhibition of STOCs is due to the blockade of chloro on both BKs and ryanodine receptors (RyRs). We also found that low concentrations of chloro resulted in additional contractions in tracheal rings that were precontracted by acetylcholine (ACH). Increases in chloro concentration reversed the contractile actions to relaxations. In the presence of IbTx or paxilline (pax), BK blockers, chloro-induced contractions were inhibited, although the high concentrations of chloro-induced relaxations were not affected. Taken together, our results indicate that chloro blocks BKs and RyRs, resulting in abolishment of STOCs and occurrence of contraction, the latter will counteract the relaxations induced by high concentrations of chloro. </AbstractText>
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Involvement of large-conductance Ca2+-activated K+ channels in chloroquine-induced force alterations in pre-contracted airway smooth muscle.

Involvement of large-conductance Ca2+-activated K+ channels in chloroquine-induced force alterations in pre-contracted airway smooth muscle.

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