NDLI: Dual effect of nitric oxide on ATP-sensitive K+ channels in rat pancreatic β cells

Content Provider	Springer Nature Link
Author	Suuchi, Takaaki Suzuki, Kimiaki Nakayama, Koichi Ishikawa, Tomohisa
Copyright Year	2008
Abstract	We have previously shown that NO has stimulatory and inhibitory effects on insulin secretion at low and high concentrations, respectively. The present study investigated effects of NO on KATP channels of rat β cells by patch clamp analysis to elucidate the mechanism for the dual effect. NOC7 at 0.5 μM suppressed KATP channels activated by diazoxide in the cell-attached and perforated whole-cell modes but failed to suppress them in the inside-out mode. The inhibitory effect in the cell-attached mode was abolished by the soluble guanylate cyclase inhibitor ODQ and by the protein kinase G inhibitor KT5823. Moreover, 0.5 μM NOC7 failed to suppress the channel activity in the presence of the mitochondrial uncoupler FCCP. In contrast, 10 μM NOC7 activated KATP channels in the cell-attached and perforated whole-cell modes, although it had no effect on the channels in the inside-out mode. The KATP currents evoked by 10 μM NOC7 in the cell-attached mode were not inhibited by ODQ. The dual effect of NOC7 at 0.5 and 10 μM was observed in the same patch. Taken together, these results suggest that low-concentration NO exerts an inhibitory effect on KATP channels of β cells, which is induced through the cGMP/protein kinase G pathway, whereas high-concentration NO activates KATP channels through the mechanism independent of cGMP.
Starting Page	573
Ending Page	579
Page Count	7
File Format	PDF
ISSN	00316768
Journal	Pflügers Archiv
Volume Number	456
Issue Number	3
e-ISSN	14322013
Language	English
Publisher	Springer-Verlag
Publisher Date	2008-02-01
Publisher Place	Berlin, Heidelberg
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Patch clamp Pancreatic β cell K+ currents NO cGMP Single channel ATP Human Physiology
Content Type	Text
Resource Type	Article
Subject	Physiology Physiology (medical) Clinical Biochemistry

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