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首页> 外文期刊>European Journal of Pharmacology: An International Journal >Effects of K+ channel openers on spontaneous action potentials in detrusor smooth muscle of the guinea-pig urinary bladder
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Effects of K+ channel openers on spontaneous action potentials in detrusor smooth muscle of the guinea-pig urinary bladder

机译：K +通道开放剂对豚鼠膀胱逼尿肌平滑肌自发动作电位的影响

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摘要

The modulation of spontaneous excitability in detrusor smooth muscle (DSM) upon the pharmacological activation of different populations of K+ channels was investigated. Effects of distinct K+ channel openers on spontaneous action potentials in DSM of the guinea-pig bladder were examined using intracellular microelectrode techniques. NS1619 (10 mu M), a large conductance Ca2+-activated K+ (BK) channel opener, transiently increased action potential frequency and then prevented their generation without hyperpolarizing the membrane in a manner sensitive to iberiotoxin (IbTX, 100 nM). A higher concentration of NS1619 (30 mu M) hyperpolarized the membrane and abolished action potential firing. NS309 (10 mu M) and SKA31 (100 mu M), small conductance Ca2+-activated K+ (SK) channel openers, dramatically increased the duration of the after-hyperpolarization and then abolished action potential firing in an apamin (100 nM)-sensitive manner. Flupirtine (10 mu M), a Kv7 channel opener, inhibited action potential firing without hyperpolarizing the membrane in a manner sensitive to XE991 (10 mu M), a Kv7 channel blocker. BRL37344 (10 mu M), a beta(3)-adrenceptor agonist, or rolipram (10 nM), a phosphodiesterase 4 inhibitor, also inhibited action potential firing. A higher concentration of rolipram (100 nM) hyperpolarized the DSM and abolished the action potentials. IbTX (100 nM) prevented the rolipram-induced blockade of action potentials but not the hyperpolarization. BK and Kv7 channels appear to predominantly contribute to the stabilization of DSM excitability. Spare SK channels could be pharmacologically activated to suppress DSM excitability. BK channels appear to be involved in the cyclic AMP induced inhibition of action potentials but not the membrane hyperpolarization. (C) 2016 Elsevier B.V. All rights reserved.
机译：研究了不同K +通道人群的药理学激活后逼尿肌平滑肌（DSM）自发兴奋性的调节。使用细胞内微电极技术检查了不同的K +通道开放剂对豚鼠膀胱DSM中自发动作电位的影响。 NS1619（10μM）是一个大电导的Ca2 +激活的K +（BK）通道开放剂，可瞬时增加动作电位频率，然后阻止其生成，而不会以对埃博毒素（IbTX，100 nM）敏感的方式使膜超极化。较高浓度的NS1619（30μM）使膜超极化，并取消了动作电位放电。 NS309（10μM）和SKA31（100μM），小的电导Ca2 +激活的K +（SK）通道开放剂，显着增加了超极化后的持续时间，然后取消了对罂粟碱（100 nM）敏感的动作电位激发方式。氟吡汀（10μM）是一种Kv7通道阻断剂，它以对Kv7通道阻断剂XE991（10μM）敏感的方式抑制了动作电位的发射，而不会使膜超极化。 BRL37344（10μM），β（3）-肾上腺素能激动剂，或咯利普兰（10 nM），磷酸二酯酶4抑制剂，也抑制动作电位放电。更高浓度的咯利普兰（100 nM）使DSM超极化并消除了动作电位。 IbTX（100 nM）阻止了咯利普兰诱导的动作电位阻断，但没有阻止超极化。 BK和Kv7通道似乎主要有助于稳定DSM的兴奋性。备用SK通道可通过药理学激活以抑制DSM兴奋性。 BK通道似乎与循环AMP诱导的动作电位抑制有关，但与膜超极化无关。 （C）2016 Elsevier B.V.保留所有权利。

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