Bisoprolol, known to be a selective β 1 -receptor antagonist, differentially but directly suppresses i K(M) and i K(erg) in pituitary cells and hippocampal neurons

Edmund Cheung So, Ning Ping Foo, Shun Yao Ko, Sheng Nan Wu

研究成果: Article

摘要

Bisoprolol (BIS) is a selective antagonist of β 1 adrenergic receptors. We examined the effects of BIS on M-type K + currents (I K(M) ) orerg-mediated K + currents (I K(erg) ) in pituitary GH 3, R1220 cells, and hippocampal mHippoE-14 cells. As GH 3 cells were exposed to BIS, amplitude of I K(M) was suppressed with an IC 50 value of 1.21 μM. The BIS-induced suppression of I K(M) 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 + (K M ) channels, along with decreased mean opening time of the channel. BIS decreased I K(erg) amplitude with an IC 50 value of 6.42 μM. Further addition of PD-118057 attenuated BIS-mediated inhibition of I K(erg) . Under current-clamp conditions, BIS depolarization increased the firing of spontaneous action potentials in GH 3 cells; addition of flupirtine, but not ractopamine, reversed BIS-induced firing rate. In R1220 cells, BIS suppressed I K(M) ; subsequent application of ML-213(Kv7.2 channel activator) reversed BIS-induced suppression of the current. In hippocampal mHippoE-14 neurons, BIS inhibited I K(M) to a greater extent compared to its depressant effect on I K(erg) . This demonstrated that in pituitary cells and hippocampal neurons the presence of BIS is capable of directly and differentially suppressing I K(M) and I K(erg) , despite its antagonism of β 1 -adrenergic receptors.

原文English
文章編號657
期刊International journal of molecular sciences
20
發行號3
DOIs
出版狀態Published - 2019 二月 2

指紋

Bisoprolol
neurons
Neurons
Depolarization
Clamping devices
cells
adrenergics
flupirtine
ractopamine
depressants
retarding
clamps
ivabradine
Adrenergic Receptors
depolarization
Adrenergic Antagonists
Isoproterenol

All Science Journal Classification (ASJC) codes

  • Catalysis
  • Molecular Biology
  • Spectroscopy
  • Computer Science Applications
  • Physical and Theoretical Chemistry
  • Organic Chemistry
  • Inorganic Chemistry

引用此文

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title = "Bisoprolol, known to be a selective β 1 -receptor antagonist, differentially but directly suppresses i K(M) and i K(erg) in pituitary cells and hippocampal neurons",
abstract = "Bisoprolol (BIS) is a selective antagonist of β 1 adrenergic receptors. We examined the effects of BIS on M-type K + currents (I K(M) ) orerg-mediated K + currents (I K(erg) ) in pituitary GH 3, R1220 cells, and hippocampal mHippoE-14 cells. As GH 3 cells were exposed to BIS, amplitude of I K(M) was suppressed with an IC 50 value of 1.21 μM. The BIS-induced suppression of I K(M) 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 + (K M ) channels, along with decreased mean opening time of the channel. BIS decreased I K(erg) amplitude with an IC 50 value of 6.42 μM. Further addition of PD-118057 attenuated BIS-mediated inhibition of I K(erg) . Under current-clamp conditions, BIS depolarization increased the firing of spontaneous action potentials in GH 3 cells; addition of flupirtine, but not ractopamine, reversed BIS-induced firing rate. In R1220 cells, BIS suppressed I K(M) ; subsequent application of ML-213(Kv7.2 channel activator) reversed BIS-induced suppression of the current. In hippocampal mHippoE-14 neurons, BIS inhibited I K(M) to a greater extent compared to its depressant effect on I K(erg) . This demonstrated that in pituitary cells and hippocampal neurons the presence of BIS is capable of directly and differentially suppressing I K(M) and I K(erg) , despite its antagonism of β 1 -adrenergic receptors.",
author = "So, {Edmund Cheung} and Foo, {Ning Ping} and Ko, {Shun Yao} and Wu, {Sheng Nan}",
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T1 - Bisoprolol, known to be a selective β 1 -receptor antagonist, differentially but directly suppresses i K(M) and i K(erg) in pituitary cells and hippocampal neurons

AU - So, Edmund Cheung

AU - Foo, Ning Ping

AU - Ko, Shun Yao

AU - Wu, Sheng Nan

PY - 2019/2/2

Y1 - 2019/2/2

N2 - Bisoprolol (BIS) is a selective antagonist of β 1 adrenergic receptors. We examined the effects of BIS on M-type K + currents (I K(M) ) orerg-mediated K + currents (I K(erg) ) in pituitary GH 3, R1220 cells, and hippocampal mHippoE-14 cells. As GH 3 cells were exposed to BIS, amplitude of I K(M) was suppressed with an IC 50 value of 1.21 μM. The BIS-induced suppression of I K(M) 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 + (K M ) channels, along with decreased mean opening time of the channel. BIS decreased I K(erg) amplitude with an IC 50 value of 6.42 μM. Further addition of PD-118057 attenuated BIS-mediated inhibition of I K(erg) . Under current-clamp conditions, BIS depolarization increased the firing of spontaneous action potentials in GH 3 cells; addition of flupirtine, but not ractopamine, reversed BIS-induced firing rate. In R1220 cells, BIS suppressed I K(M) ; subsequent application of ML-213(Kv7.2 channel activator) reversed BIS-induced suppression of the current. In hippocampal mHippoE-14 neurons, BIS inhibited I K(M) to a greater extent compared to its depressant effect on I K(erg) . This demonstrated that in pituitary cells and hippocampal neurons the presence of BIS is capable of directly and differentially suppressing I K(M) and I K(erg) , despite its antagonism of β 1 -adrenergic receptors.

AB - Bisoprolol (BIS) is a selective antagonist of β 1 adrenergic receptors. We examined the effects of BIS on M-type K + currents (I K(M) ) orerg-mediated K + currents (I K(erg) ) in pituitary GH 3, R1220 cells, and hippocampal mHippoE-14 cells. As GH 3 cells were exposed to BIS, amplitude of I K(M) was suppressed with an IC 50 value of 1.21 μM. The BIS-induced suppression of I K(M) 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 + (K M ) channels, along with decreased mean opening time of the channel. BIS decreased I K(erg) amplitude with an IC 50 value of 6.42 μM. Further addition of PD-118057 attenuated BIS-mediated inhibition of I K(erg) . Under current-clamp conditions, BIS depolarization increased the firing of spontaneous action potentials in GH 3 cells; addition of flupirtine, but not ractopamine, reversed BIS-induced firing rate. In R1220 cells, BIS suppressed I K(M) ; subsequent application of ML-213(Kv7.2 channel activator) reversed BIS-induced suppression of the current. In hippocampal mHippoE-14 neurons, BIS inhibited I K(M) to a greater extent compared to its depressant effect on I K(erg) . This demonstrated that in pituitary cells and hippocampal neurons the presence of BIS is capable of directly and differentially suppressing I K(M) and I K(erg) , despite its antagonism of β 1 -adrenergic receptors.

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U2 - 10.3390/ijms20030657

DO - 10.3390/ijms20030657

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