Bisoprolol, Known to Be a Selective β<sub<1</sub<-Receptor Antagonist, Differentially but Directly Suppresses I<sub<K(M)</sub< and I<sub<K(erg)</sub< in Pituitary Cells and Hippocampal Neurons

Bisoprolol (BIS) is a selective antagonist of β<sub<1</sub< adrenergic receptors. We examined the effects of BIS on M-type K<sup<+</sup< currents (I<sub<K(M)</sub<) or <i<erg</i<-mediated K<sup<+</sup< currents (I<sub<K(erg)</sub&l...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Edmund Cheung So [verfasserIn] Ning-Ping Foo [verfasserIn] Shun Yao Ko [verfasserIn] Sheng-Nan Wu [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2019

Schlagwörter:	bisoprolol M-type K M-type K membrane potential pituitary cell

Übergeordnetes Werk:	In: International Journal of Molecular Sciences - MDPI AG, 2003, 20(2019), 3, p 657
Übergeordnetes Werk:	volume:20 ; year:2019 ; number:3, p 657

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3390/ijms20030657

Katalog-ID:	DOAJ079755054

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520			\|a Bisoprolol (BIS) is a selective antagonist of β<sub<1</sub< adrenergic receptors. We examined the effects of BIS on M-type K<sup<+</sup< currents (I<sub<K(M)</sub<) or <i<erg</i<-mediated K<sup<+</sup< currents (I<sub<K(erg)</sub<) in pituitary GH<sub<3,</sub< R1220 cells, and hippocampal mHippoE-14 cells. As GH<sub<3</sub< cells were exposed to BIS, amplitude of I<sub<K(M)</sub< was suppressed with an IC<sub<50</sub< value of 1.21 μM. The BIS-induced suppression of I<sub<K(M)</sub< amplitude was not affected by addition of isoproterenol or ractopamine, but attenuated by flupirtine or ivabradine. In cell-attached current, BIS decreased the open probability of M-type K<sup<+</sup< (K<sub<M</sub<) channels, along with decreased mean opening time of the channel. BIS decreased I<sub<K(erg)</sub< amplitude with an IC<sub<50</sub< value of 6.42 μM. Further addition of PD-118057 attenuated BIS-mediated inhibition of I<sub<K(erg)</sub<. Under current-clamp conditions, BIS depolarization increased the firing of spontaneous action potentials in GH<sub<3</sub< cells; addition of flupirtine, but not ractopamine, reversed BIS-induced firing rate. In R1220 cells, BIS suppressed I<sub<K(M)</sub<; subsequent application of ML-213(Kv7.2 channel activator) reversed BIS-induced suppression of the current. In hippocampal mHippoE-14 neurons, BIS inhibited I<sub<K(M)</sub< to a greater extent compared to its depressant effect on I<sub<K(erg)</sub<. This demonstrated that in pituitary cells and hippocampal neurons the presence of BIS is capable of directly and differentially suppressing I<sub<K(M)</sub< and I<sub<K(erg)</sub<, despite its antagonism of β<sub<1</sub<-adrenergic receptors.
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author_variant	e c s ecs n p f npf s y k syk s n w snw
matchkey_str	article:14220067:2019----::iorllnwtbaeetvsbsbeetrnaoitifrnilyudrclsprseiuksbniukrs
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allfields	10.3390/ijms20030657 doi (DE-627)DOAJ079755054 (DE-599)DOAJ7291b4fcc88f489a932ea6068ec7512a DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Edmund Cheung So verfasserin aut Bisoprolol, Known to Be a Selective β<sub<1</sub<-Receptor Antagonist, Differentially but Directly Suppresses I<sub<K(M)</sub< and I<sub<K(erg)</sub< in Pituitary Cells and Hippocampal Neurons 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Bisoprolol (BIS) is a selective antagonist of β<sub<1</sub< adrenergic receptors. We examined the effects of BIS on M-type K<sup<+</sup< currents (I<sub<K(M)</sub<) or <i<erg</i<-mediated K<sup<+</sup< currents (I<sub<K(erg)</sub<) in pituitary GH<sub<3,</sub< R1220 cells, and hippocampal mHippoE-14 cells. As GH<sub<3</sub< cells were exposed to BIS, amplitude of I<sub<K(M)</sub< was suppressed with an IC<sub<50</sub< value of 1.21 μM. The BIS-induced suppression of I<sub<K(M)</sub< amplitude was not affected by addition of isoproterenol or ractopamine, but attenuated by flupirtine or ivabradine. In cell-attached current, BIS decreased the open probability of M-type K<sup<+</sup< (K<sub<M</sub<) channels, along with decreased mean opening time of the channel. BIS decreased I<sub<K(erg)</sub< amplitude with an IC<sub<50</sub< value of 6.42 μM. Further addition of PD-118057 attenuated BIS-mediated inhibition of I<sub<K(erg)</sub<. Under current-clamp conditions, BIS depolarization increased the firing of spontaneous action potentials in GH<sub<3</sub< cells; addition of flupirtine, but not ractopamine, reversed BIS-induced firing rate. In R1220 cells, BIS suppressed I<sub<K(M)</sub<; subsequent application of ML-213(Kv7.2 channel activator) reversed BIS-induced suppression of the current. In hippocampal mHippoE-14 neurons, BIS inhibited I<sub<K(M)</sub< to a greater extent compared to its depressant effect on I<sub<K(erg)</sub<. This demonstrated that in pituitary cells and hippocampal neurons the presence of BIS is capable of directly and differentially suppressing I<sub<K(M)</sub< and I<sub<K(erg)</sub<, despite its antagonism of β<sub<1</sub<-adrenergic receptors. bisoprolol M-type K<sup<+</sup< current M-type K<sup<+</sup< channel. erg-mediated K<sup<+</sup< current membrane potential pituitary cell Biology (General) Chemistry Ning-Ping Foo verfasserin aut Shun Yao Ko verfasserin aut Sheng-Nan Wu verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 20(2019), 3, p 657 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:20 year:2019 number:3, p 657 https://doi.org/10.3390/ijms20030657 kostenfrei https://doaj.org/article/7291b4fcc88f489a932ea6068ec7512a kostenfrei https://www.mdpi.com/1422-0067/20/3/657 kostenfrei https://doaj.org/toc/1422-0067 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 20 2019 3, p 657
spelling	10.3390/ijms20030657 doi (DE-627)DOAJ079755054 (DE-599)DOAJ7291b4fcc88f489a932ea6068ec7512a DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Edmund Cheung So verfasserin aut Bisoprolol, Known to Be a Selective β<sub<1</sub<-Receptor Antagonist, Differentially but Directly Suppresses I<sub<K(M)</sub< and I<sub<K(erg)</sub< in Pituitary Cells and Hippocampal Neurons 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Bisoprolol (BIS) is a selective antagonist of β<sub<1</sub< adrenergic receptors. We examined the effects of BIS on M-type K<sup<+</sup< currents (I<sub<K(M)</sub<) or <i<erg</i<-mediated K<sup<+</sup< currents (I<sub<K(erg)</sub<) in pituitary GH<sub<3,</sub< R1220 cells, and hippocampal mHippoE-14 cells. As GH<sub<3</sub< cells were exposed to BIS, amplitude of I<sub<K(M)</sub< was suppressed with an IC<sub<50</sub< value of 1.21 μM. The BIS-induced suppression of I<sub<K(M)</sub< amplitude was not affected by addition of isoproterenol or ractopamine, but attenuated by flupirtine or ivabradine. In cell-attached current, BIS decreased the open probability of M-type K<sup<+</sup< (K<sub<M</sub<) channels, along with decreased mean opening time of the channel. BIS decreased I<sub<K(erg)</sub< amplitude with an IC<sub<50</sub< value of 6.42 μM. Further addition of PD-118057 attenuated BIS-mediated inhibition of I<sub<K(erg)</sub<. Under current-clamp conditions, BIS depolarization increased the firing of spontaneous action potentials in GH<sub<3</sub< cells; addition of flupirtine, but not ractopamine, reversed BIS-induced firing rate. In R1220 cells, BIS suppressed I<sub<K(M)</sub<; subsequent application of ML-213(Kv7.2 channel activator) reversed BIS-induced suppression of the current. In hippocampal mHippoE-14 neurons, BIS inhibited I<sub<K(M)</sub< to a greater extent compared to its depressant effect on I<sub<K(erg)</sub<. This demonstrated that in pituitary cells and hippocampal neurons the presence of BIS is capable of directly and differentially suppressing I<sub<K(M)</sub< and I<sub<K(erg)</sub<, despite its antagonism of β<sub<1</sub<-adrenergic receptors. bisoprolol M-type K<sup<+</sup< current M-type K<sup<+</sup< channel. erg-mediated K<sup<+</sup< current membrane potential pituitary cell Biology (General) Chemistry Ning-Ping Foo verfasserin aut Shun Yao Ko verfasserin aut Sheng-Nan Wu verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 20(2019), 3, p 657 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:20 year:2019 number:3, p 657 https://doi.org/10.3390/ijms20030657 kostenfrei https://doaj.org/article/7291b4fcc88f489a932ea6068ec7512a kostenfrei https://www.mdpi.com/1422-0067/20/3/657 kostenfrei https://doaj.org/toc/1422-0067 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 20 2019 3, p 657
allfields_unstemmed	10.3390/ijms20030657 doi (DE-627)DOAJ079755054 (DE-599)DOAJ7291b4fcc88f489a932ea6068ec7512a DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Edmund Cheung So verfasserin aut Bisoprolol, Known to Be a Selective β<sub<1</sub<-Receptor Antagonist, Differentially but Directly Suppresses I<sub<K(M)</sub< and I<sub<K(erg)</sub< in Pituitary Cells and Hippocampal Neurons 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Bisoprolol (BIS) is a selective antagonist of β<sub<1</sub< adrenergic receptors. We examined the effects of BIS on M-type K<sup<+</sup< currents (I<sub<K(M)</sub<) or <i<erg</i<-mediated K<sup<+</sup< currents (I<sub<K(erg)</sub<) in pituitary GH<sub<3,</sub< R1220 cells, and hippocampal mHippoE-14 cells. As GH<sub<3</sub< cells were exposed to BIS, amplitude of I<sub<K(M)</sub< was suppressed with an IC<sub<50</sub< value of 1.21 μM. The BIS-induced suppression of I<sub<K(M)</sub< amplitude was not affected by addition of isoproterenol or ractopamine, but attenuated by flupirtine or ivabradine. In cell-attached current, BIS decreased the open probability of M-type K<sup<+</sup< (K<sub<M</sub<) channels, along with decreased mean opening time of the channel. BIS decreased I<sub<K(erg)</sub< amplitude with an IC<sub<50</sub< value of 6.42 μM. Further addition of PD-118057 attenuated BIS-mediated inhibition of I<sub<K(erg)</sub<. Under current-clamp conditions, BIS depolarization increased the firing of spontaneous action potentials in GH<sub<3</sub< cells; addition of flupirtine, but not ractopamine, reversed BIS-induced firing rate. In R1220 cells, BIS suppressed I<sub<K(M)</sub<; subsequent application of ML-213(Kv7.2 channel activator) reversed BIS-induced suppression of the current. In hippocampal mHippoE-14 neurons, BIS inhibited I<sub<K(M)</sub< to a greater extent compared to its depressant effect on I<sub<K(erg)</sub<. This demonstrated that in pituitary cells and hippocampal neurons the presence of BIS is capable of directly and differentially suppressing I<sub<K(M)</sub< and I<sub<K(erg)</sub<, despite its antagonism of β<sub<1</sub<-adrenergic receptors. bisoprolol M-type K<sup<+</sup< current M-type K<sup<+</sup< channel. erg-mediated K<sup<+</sup< current membrane potential pituitary cell Biology (General) Chemistry Ning-Ping Foo verfasserin aut Shun Yao Ko verfasserin aut Sheng-Nan Wu verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 20(2019), 3, p 657 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:20 year:2019 number:3, p 657 https://doi.org/10.3390/ijms20030657 kostenfrei https://doaj.org/article/7291b4fcc88f489a932ea6068ec7512a kostenfrei https://www.mdpi.com/1422-0067/20/3/657 kostenfrei https://doaj.org/toc/1422-0067 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 20 2019 3, p 657
allfieldsGer	10.3390/ijms20030657 doi (DE-627)DOAJ079755054 (DE-599)DOAJ7291b4fcc88f489a932ea6068ec7512a DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Edmund Cheung So verfasserin aut Bisoprolol, Known to Be a Selective β<sub<1</sub<-Receptor Antagonist, Differentially but Directly Suppresses I<sub<K(M)</sub< and I<sub<K(erg)</sub< in Pituitary Cells and Hippocampal Neurons 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Bisoprolol (BIS) is a selective antagonist of β<sub<1</sub< adrenergic receptors. We examined the effects of BIS on M-type K<sup<+</sup< currents (I<sub<K(M)</sub<) or <i<erg</i<-mediated K<sup<+</sup< currents (I<sub<K(erg)</sub<) in pituitary GH<sub<3,</sub< R1220 cells, and hippocampal mHippoE-14 cells. As GH<sub<3</sub< cells were exposed to BIS, amplitude of I<sub<K(M)</sub< was suppressed with an IC<sub<50</sub< value of 1.21 μM. The BIS-induced suppression of I<sub<K(M)</sub< amplitude was not affected by addition of isoproterenol or ractopamine, but attenuated by flupirtine or ivabradine. In cell-attached current, BIS decreased the open probability of M-type K<sup<+</sup< (K<sub<M</sub<) channels, along with decreased mean opening time of the channel. BIS decreased I<sub<K(erg)</sub< amplitude with an IC<sub<50</sub< value of 6.42 μM. Further addition of PD-118057 attenuated BIS-mediated inhibition of I<sub<K(erg)</sub<. Under current-clamp conditions, BIS depolarization increased the firing of spontaneous action potentials in GH<sub<3</sub< cells; addition of flupirtine, but not ractopamine, reversed BIS-induced firing rate. In R1220 cells, BIS suppressed I<sub<K(M)</sub<; subsequent application of ML-213(Kv7.2 channel activator) reversed BIS-induced suppression of the current. In hippocampal mHippoE-14 neurons, BIS inhibited I<sub<K(M)</sub< to a greater extent compared to its depressant effect on I<sub<K(erg)</sub<. This demonstrated that in pituitary cells and hippocampal neurons the presence of BIS is capable of directly and differentially suppressing I<sub<K(M)</sub< and I<sub<K(erg)</sub<, despite its antagonism of β<sub<1</sub<-adrenergic receptors. bisoprolol M-type K<sup<+</sup< current M-type K<sup<+</sup< channel. erg-mediated K<sup<+</sup< current membrane potential pituitary cell Biology (General) Chemistry Ning-Ping Foo verfasserin aut Shun Yao Ko verfasserin aut Sheng-Nan Wu verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 20(2019), 3, p 657 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:20 year:2019 number:3, p 657 https://doi.org/10.3390/ijms20030657 kostenfrei https://doaj.org/article/7291b4fcc88f489a932ea6068ec7512a kostenfrei https://www.mdpi.com/1422-0067/20/3/657 kostenfrei https://doaj.org/toc/1422-0067 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 20 2019 3, p 657
allfieldsSound	10.3390/ijms20030657 doi (DE-627)DOAJ079755054 (DE-599)DOAJ7291b4fcc88f489a932ea6068ec7512a DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Edmund Cheung So verfasserin aut Bisoprolol, Known to Be a Selective β<sub<1</sub<-Receptor Antagonist, Differentially but Directly Suppresses I<sub<K(M)</sub< and I<sub<K(erg)</sub< in Pituitary Cells and Hippocampal Neurons 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Bisoprolol (BIS) is a selective antagonist of β<sub<1</sub< adrenergic receptors. We examined the effects of BIS on M-type K<sup<+</sup< currents (I<sub<K(M)</sub<) or <i<erg</i<-mediated K<sup<+</sup< currents (I<sub<K(erg)</sub<) in pituitary GH<sub<3,</sub< R1220 cells, and hippocampal mHippoE-14 cells. As GH<sub<3</sub< cells were exposed to BIS, amplitude of I<sub<K(M)</sub< was suppressed with an IC<sub<50</sub< value of 1.21 μM. The BIS-induced suppression of I<sub<K(M)</sub< amplitude was not affected by addition of isoproterenol or ractopamine, but attenuated by flupirtine or ivabradine. In cell-attached current, BIS decreased the open probability of M-type K<sup<+</sup< (K<sub<M</sub<) channels, along with decreased mean opening time of the channel. BIS decreased I<sub<K(erg)</sub< amplitude with an IC<sub<50</sub< value of 6.42 μM. Further addition of PD-118057 attenuated BIS-mediated inhibition of I<sub<K(erg)</sub<. Under current-clamp conditions, BIS depolarization increased the firing of spontaneous action potentials in GH<sub<3</sub< cells; addition of flupirtine, but not ractopamine, reversed BIS-induced firing rate. In R1220 cells, BIS suppressed I<sub<K(M)</sub<; subsequent application of ML-213(Kv7.2 channel activator) reversed BIS-induced suppression of the current. In hippocampal mHippoE-14 neurons, BIS inhibited I<sub<K(M)</sub< to a greater extent compared to its depressant effect on I<sub<K(erg)</sub<. This demonstrated that in pituitary cells and hippocampal neurons the presence of BIS is capable of directly and differentially suppressing I<sub<K(M)</sub< and I<sub<K(erg)</sub<, despite its antagonism of β<sub<1</sub<-adrenergic receptors. bisoprolol M-type K<sup<+</sup< current M-type K<sup<+</sup< channel. erg-mediated K<sup<+</sup< current membrane potential pituitary cell Biology (General) Chemistry Ning-Ping Foo verfasserin aut Shun Yao Ko verfasserin aut Sheng-Nan Wu verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 20(2019), 3, p 657 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:20 year:2019 number:3, p 657 https://doi.org/10.3390/ijms20030657 kostenfrei https://doaj.org/article/7291b4fcc88f489a932ea6068ec7512a kostenfrei https://www.mdpi.com/1422-0067/20/3/657 kostenfrei https://doaj.org/toc/1422-0067 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 20 2019 3, p 657
language	English
source	In International Journal of Molecular Sciences 20(2019), 3, p 657 volume:20 year:2019 number:3, p 657
sourceStr	In International Journal of Molecular Sciences 20(2019), 3, p 657 volume:20 year:2019 number:3, p 657
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	bisoprolol M-type K<sup<+</sup< current M-type K<sup<+</sup< channel. erg-mediated K<sup<+</sup< current membrane potential pituitary cell Biology (General) Chemistry
isfreeaccess_bool	true
container_title	International Journal of Molecular Sciences
authorswithroles_txt_mv	Edmund Cheung So @@aut@@ Ning-Ping Foo @@aut@@ Shun Yao Ko @@aut@@ Sheng-Nan Wu @@aut@@
publishDateDaySort_date	2019-01-01T00:00:00Z
hierarchy_top_id	316340715
id	DOAJ079755054
language_de	englisch
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callnumber-first	Q - Science
author	Edmund Cheung So
spellingShingle	Edmund Cheung So misc QH301-705.5 misc QD1-999 misc bisoprolol misc M-type K<sup<+</sup< current misc M-type K<sup<+</sup< channel. erg-mediated K<sup<+</sup< current misc membrane potential misc pituitary cell misc Biology (General) misc Chemistry Bisoprolol, Known to Be a Selective β<sub<1</sub<-Receptor Antagonist, Differentially but Directly Suppresses I<sub<K(M)</sub< and I<sub<K(erg)</sub< in Pituitary Cells and Hippocampal Neurons
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topic_title	QH301-705.5 QD1-999 Bisoprolol, Known to Be a Selective β<sub<1</sub<-Receptor Antagonist, Differentially but Directly Suppresses I<sub<K(M)</sub< and I<sub<K(erg)</sub< in Pituitary Cells and Hippocampal Neurons bisoprolol M-type K<sup<+</sup< current M-type K<sup<+</sup< channel. erg-mediated K<sup<+</sup< current membrane potential pituitary cell
topic	misc QH301-705.5 misc QD1-999 misc bisoprolol misc M-type K<sup<+</sup< current misc M-type K<sup<+</sup< channel. erg-mediated K<sup<+</sup< current misc membrane potential misc pituitary cell misc Biology (General) misc Chemistry
topic_unstemmed	misc QH301-705.5 misc QD1-999 misc bisoprolol misc M-type K<sup<+</sup< current misc M-type K<sup<+</sup< channel. erg-mediated K<sup<+</sup< current misc membrane potential misc pituitary cell misc Biology (General) misc Chemistry
topic_browse	misc QH301-705.5 misc QD1-999 misc bisoprolol misc M-type K<sup<+</sup< current misc M-type K<sup<+</sup< channel. erg-mediated K<sup<+</sup< current misc membrane potential misc pituitary cell misc Biology (General) misc Chemistry
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title	Bisoprolol, Known to Be a Selective β<sub<1</sub<-Receptor Antagonist, Differentially but Directly Suppresses I<sub<K(M)</sub< and I<sub<K(erg)</sub< in Pituitary Cells and Hippocampal Neurons
ctrlnum	(DE-627)DOAJ079755054 (DE-599)DOAJ7291b4fcc88f489a932ea6068ec7512a
title_full	Bisoprolol, Known to Be a Selective β<sub<1</sub<-Receptor Antagonist, Differentially but Directly Suppresses I<sub<K(M)</sub< and I<sub<K(erg)</sub< in Pituitary Cells and Hippocampal Neurons
author_sort	Edmund Cheung So
journal	International Journal of Molecular Sciences
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author_browse	Edmund Cheung So Ning-Ping Foo Shun Yao Ko Sheng-Nan Wu
container_volume	20
class	QH301-705.5 QD1-999
format_se	Elektronische Aufsätze
author-letter	Edmund Cheung So
doi_str_mv	10.3390/ijms20030657
author2-role	verfasserin
title_sort	bisoprolol, known to be a selective β<sub<1</sub<-receptor antagonist, differentially but directly suppresses i<sub<k(m)</sub< and i<sub<k(erg)</sub< in pituitary cells and hippocampal neurons
callnumber	QH301-705.5
title_auth	Bisoprolol, Known to Be a Selective β<sub<1</sub<-Receptor Antagonist, Differentially but Directly Suppresses I<sub<K(M)</sub< and I<sub<K(erg)</sub< in Pituitary Cells and Hippocampal Neurons
abstract	Bisoprolol (BIS) is a selective antagonist of β<sub<1</sub< adrenergic receptors. We examined the effects of BIS on M-type K<sup<+</sup< currents (I<sub<K(M)</sub<) or <i<erg</i<-mediated K<sup<+</sup< currents (I<sub<K(erg)</sub<) in pituitary GH<sub<3,</sub< R1220 cells, and hippocampal mHippoE-14 cells. As GH<sub<3</sub< cells were exposed to BIS, amplitude of I<sub<K(M)</sub< was suppressed with an IC<sub<50</sub< value of 1.21 μM. The BIS-induced suppression of I<sub<K(M)</sub< amplitude was not affected by addition of isoproterenol or ractopamine, but attenuated by flupirtine or ivabradine. In cell-attached current, BIS decreased the open probability of M-type K<sup<+</sup< (K<sub<M</sub<) channels, along with decreased mean opening time of the channel. BIS decreased I<sub<K(erg)</sub< amplitude with an IC<sub<50</sub< value of 6.42 μM. Further addition of PD-118057 attenuated BIS-mediated inhibition of I<sub<K(erg)</sub<. Under current-clamp conditions, BIS depolarization increased the firing of spontaneous action potentials in GH<sub<3</sub< cells; addition of flupirtine, but not ractopamine, reversed BIS-induced firing rate. In R1220 cells, BIS suppressed I<sub<K(M)</sub<; subsequent application of ML-213(Kv7.2 channel activator) reversed BIS-induced suppression of the current. In hippocampal mHippoE-14 neurons, BIS inhibited I<sub<K(M)</sub< to a greater extent compared to its depressant effect on I<sub<K(erg)</sub<. This demonstrated that in pituitary cells and hippocampal neurons the presence of BIS is capable of directly and differentially suppressing I<sub<K(M)</sub< and I<sub<K(erg)</sub<, despite its antagonism of β<sub<1</sub<-adrenergic receptors.
abstractGer	Bisoprolol (BIS) is a selective antagonist of β<sub<1</sub< adrenergic receptors. We examined the effects of BIS on M-type K<sup<+</sup< currents (I<sub<K(M)</sub<) or <i<erg</i<-mediated K<sup<+</sup< currents (I<sub<K(erg)</sub<) in pituitary GH<sub<3,</sub< R1220 cells, and hippocampal mHippoE-14 cells. As GH<sub<3</sub< cells were exposed to BIS, amplitude of I<sub<K(M)</sub< was suppressed with an IC<sub<50</sub< value of 1.21 μM. The BIS-induced suppression of I<sub<K(M)</sub< amplitude was not affected by addition of isoproterenol or ractopamine, but attenuated by flupirtine or ivabradine. In cell-attached current, BIS decreased the open probability of M-type K<sup<+</sup< (K<sub<M</sub<) channels, along with decreased mean opening time of the channel. BIS decreased I<sub<K(erg)</sub< amplitude with an IC<sub<50</sub< value of 6.42 μM. Further addition of PD-118057 attenuated BIS-mediated inhibition of I<sub<K(erg)</sub<. Under current-clamp conditions, BIS depolarization increased the firing of spontaneous action potentials in GH<sub<3</sub< cells; addition of flupirtine, but not ractopamine, reversed BIS-induced firing rate. In R1220 cells, BIS suppressed I<sub<K(M)</sub<; subsequent application of ML-213(Kv7.2 channel activator) reversed BIS-induced suppression of the current. In hippocampal mHippoE-14 neurons, BIS inhibited I<sub<K(M)</sub< to a greater extent compared to its depressant effect on I<sub<K(erg)</sub<. This demonstrated that in pituitary cells and hippocampal neurons the presence of BIS is capable of directly and differentially suppressing I<sub<K(M)</sub< and I<sub<K(erg)</sub<, despite its antagonism of β<sub<1</sub<-adrenergic receptors.
abstract_unstemmed	Bisoprolol (BIS) is a selective antagonist of β<sub<1</sub< adrenergic receptors. We examined the effects of BIS on M-type K<sup<+</sup< currents (I<sub<K(M)</sub<) or <i<erg</i<-mediated K<sup<+</sup< currents (I<sub<K(erg)</sub<) in pituitary GH<sub<3,</sub< R1220 cells, and hippocampal mHippoE-14 cells. As GH<sub<3</sub< cells were exposed to BIS, amplitude of I<sub<K(M)</sub< was suppressed with an IC<sub<50</sub< value of 1.21 μM. The BIS-induced suppression of I<sub<K(M)</sub< amplitude was not affected by addition of isoproterenol or ractopamine, but attenuated by flupirtine or ivabradine. In cell-attached current, BIS decreased the open probability of M-type K<sup<+</sup< (K<sub<M</sub<) channels, along with decreased mean opening time of the channel. BIS decreased I<sub<K(erg)</sub< amplitude with an IC<sub<50</sub< value of 6.42 μM. Further addition of PD-118057 attenuated BIS-mediated inhibition of I<sub<K(erg)</sub<. Under current-clamp conditions, BIS depolarization increased the firing of spontaneous action potentials in GH<sub<3</sub< cells; addition of flupirtine, but not ractopamine, reversed BIS-induced firing rate. In R1220 cells, BIS suppressed I<sub<K(M)</sub<; subsequent application of ML-213(Kv7.2 channel activator) reversed BIS-induced suppression of the current. In hippocampal mHippoE-14 neurons, BIS inhibited I<sub<K(M)</sub< to a greater extent compared to its depressant effect on I<sub<K(erg)</sub<. This demonstrated that in pituitary cells and hippocampal neurons the presence of BIS is capable of directly and differentially suppressing I<sub<K(M)</sub< and I<sub<K(erg)</sub<, despite its antagonism of β<sub<1</sub<-adrenergic receptors.
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container_issue	3, p 657
title_short	Bisoprolol, Known to Be a Selective β<sub<1</sub<-Receptor Antagonist, Differentially but Directly Suppresses I<sub<K(M)</sub< and I<sub<K(erg)</sub< in Pituitary Cells and Hippocampal Neurons
url	https://doi.org/10.3390/ijms20030657 https://doaj.org/article/7291b4fcc88f489a932ea6068ec7512a https://www.mdpi.com/1422-0067/20/3/657 https://doaj.org/toc/1422-0067
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Bisoprolol, Known to Be a Selective β<sub<1</sub<-Receptor Antagonist, Differentially but Directly Suppresses I<sub<K(M)</sub< and I<sub<K(erg)</sub< in Pituitary Cells and Hippocampal Neurons

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