The Guanylyl Cyclase Activator YC-1 Directly Inhibits the Voltage-Dependent K+ Channels in Rabbit Coronary Arterial Smooth Muscle Cells
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概要
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We investigated the effects of YC-1, an activator of soluble guanylyl cyclase (sGC), on voltage-dependent K+ (Kv) channels in smooth muscle cells from freshly isolated rabbit coronary arteries by using the whole-cell patch clamp technique. YC-1 inhibited the Kv current in a dose-dependent fashion with an apparent Kd of 9.67 μM. It accelerated the decay rate of Kv channel inactivation without altering the kinetics of current activation. The rate constants of association and dissociation for YC-1 were 0.36 ± 0.01 μM−1−1 and 3.44 ± 0.22 s−1, respectively. YC-1 did not have a significant effect on the steady-state activation and inactivation curves. The recovery time constant from inactivation was decreased in the presence of YC-1, and application of train pulses (1 or 2 Hz) caused a progressive increase in the YC-1 blockade, indicating that YC-1–induced inhibition of Kv currents is use-dependent. Pretreatment with Bay 41-2272 (also a sGC activator), ODQ (a sGC inhibitor), or Rp-8-Br-PET-cGMPs (a protein kinase G inhibitor) did not affect the basal Kv current and also did not significantly alter the inhibitory effect of YC-1. From these results, we suggest that YC-1 directly inhibits the Kv current independently of sGC activation and in a state-, time-, and use-dependent fashion.
- 社団法人 日本薬理学会の論文
著者
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PARK Yeong-Min
Department of Microbiology & Immunology, and National Research Laboratory of Dendritic Cell Differen
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KO Eun
National Research Laboratory for Mitochondrial Signaling, FIRST Mitochondria Research Group, Departm
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HAN Jin
National Research Laboratory for Mitochondrial Signaling, FIRST Mitochondria Research Group, Departm
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JUNG In
Department of Microbiology and Immunology and National Research Laboratory of Dentritic, Cell Differ
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PARK Won
National Research Laboratory for Mitochondrial Signaling, FIRST Mitochondria Research Group, Departm
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Ko Jae-Hong
Department of Physiology, College of Medicine, Chung-Ang University, Korea
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Son Youn
Université Paris-Sud 11, Faculté de Pharmacie, France
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Hong Da
National Research Laboratory for Mitochondrial Signaling, Department of Physiology, College of Medic
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Choi Tae-Hoon
Department of Physical Education, Andong Science College, Korea
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Kim Nari
National Research Laboratory for Mitochondrial Signaling, Department of Physiology, College of Medic
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