File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Contribution of ATP-sensitive potassium channels to the electrophysiological effects of adenosine in guinea-pig atrial cells

TitleContribution of ATP-sensitive potassium channels to the electrophysiological effects of adenosine in guinea-pig atrial cells
Authors
Issue Date1995
PublisherWiley-Blackwell Publishing Ltd.. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0022-3751
Citation
Journal Of Physiology, 1995, v. 484 n. 3, p. 629-642 How to Cite?
Abstract1. Adenosine caused dose-dependent action potential abbreviation in multicellular guinea-pig atrial preparations, an action antagonized by glyburide (IC50 31 μM) in both physiological and low-chloride superfusate. 2. When 5 mM ATP was included in pipettes for whole-cell voltage clamp of isolated guinea pig atrial myocytes, adenosine (10 μM) increased the holding current at -40 mV from 41 ± 8 to 246 ± 31 pA (mean ± S.E.M., P < 0.01), and glyburide (20 μM) returned the holding current to 69 ± 11 pA (P < 0.01 vs. adenosine alone). Acetylcholine (10 μM) also increased the holding current, but its effects were not altered by glyburide. Both adenosine and acetylcholine induced an additional current component in response to 500 ms voltage steps. Glyburide partially inhibited the adenosine-induced current, but did not alter the effect of acetylcholine. In the presence of maximally effective acetylcholine concentrations, adenosine increased membrane conductance (P < 0.01), although to a lesser extent than in the absence of acetylcholine. 4. Single K+ channel activity was seen in only one of eight cell-attached patches in the absence of adenosine or acetylcholine (0.5 mM Ba2+ in bath and pipette solutions). With acetylcholine (10 μM) in the pipette, inwardly rectifying channels (conductance, 41 ± 5 pS) were seen in five of six patches. With adenosine (10 μM) in the pipette, single-channel activity was seen in twelve of fourteen patches with two populations of channels, one similar to that induced by acetylcholine and another higher-conductance channel (72 ± 5 pS) that showed less inward rectification. Glyburide (20 μM) suppressed the high-conductance channel (68 ± 2 pS) leaving a single channel type with a conductance of 36 ± 5 pS and strong inward rectification. 5. We conclude that K(ATP)+ channels contribute to the electrophysiological actions of adenosine on guinea-pig atrium in the presence of physiological intracellular ATP levels, and may therefore play a role in the cardiac electrophysiological effects of adenosine in the absence of myocardial ischaemia.
Persistent Identifierhttp://hdl.handle.net/10722/162090
ISSN
2015 Impact Factor: 4.731
2015 SCImago Journal Rankings: 2.670
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLi, GRen_US
dc.contributor.authorFeng, Jen_US
dc.contributor.authorShrier, Aen_US
dc.contributor.authorNattel, Sen_US
dc.date.accessioned2012-09-05T05:17:14Z-
dc.date.available2012-09-05T05:17:14Z-
dc.date.issued1995en_US
dc.identifier.citationJournal Of Physiology, 1995, v. 484 n. 3, p. 629-642en_US
dc.identifier.issn0022-3751en_US
dc.identifier.urihttp://hdl.handle.net/10722/162090-
dc.description.abstract1. Adenosine caused dose-dependent action potential abbreviation in multicellular guinea-pig atrial preparations, an action antagonized by glyburide (IC50 31 μM) in both physiological and low-chloride superfusate. 2. When 5 mM ATP was included in pipettes for whole-cell voltage clamp of isolated guinea pig atrial myocytes, adenosine (10 μM) increased the holding current at -40 mV from 41 ± 8 to 246 ± 31 pA (mean ± S.E.M., P < 0.01), and glyburide (20 μM) returned the holding current to 69 ± 11 pA (P < 0.01 vs. adenosine alone). Acetylcholine (10 μM) also increased the holding current, but its effects were not altered by glyburide. Both adenosine and acetylcholine induced an additional current component in response to 500 ms voltage steps. Glyburide partially inhibited the adenosine-induced current, but did not alter the effect of acetylcholine. In the presence of maximally effective acetylcholine concentrations, adenosine increased membrane conductance (P < 0.01), although to a lesser extent than in the absence of acetylcholine. 4. Single K+ channel activity was seen in only one of eight cell-attached patches in the absence of adenosine or acetylcholine (0.5 mM Ba2+ in bath and pipette solutions). With acetylcholine (10 μM) in the pipette, inwardly rectifying channels (conductance, 41 ± 5 pS) were seen in five of six patches. With adenosine (10 μM) in the pipette, single-channel activity was seen in twelve of fourteen patches with two populations of channels, one similar to that induced by acetylcholine and another higher-conductance channel (72 ± 5 pS) that showed less inward rectification. Glyburide (20 μM) suppressed the high-conductance channel (68 ± 2 pS) leaving a single channel type with a conductance of 36 ± 5 pS and strong inward rectification. 5. We conclude that K(ATP)+ channels contribute to the electrophysiological actions of adenosine on guinea-pig atrium in the presence of physiological intracellular ATP levels, and may therefore play a role in the cardiac electrophysiological effects of adenosine in the absence of myocardial ischaemia.en_US
dc.languageengen_US
dc.publisherWiley-Blackwell Publishing Ltd.. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0022-3751en_US
dc.relation.ispartofJournal of Physiologyen_US
dc.subject.meshAcetylcholine - Pharmacologyen_US
dc.subject.meshAction Potentials - Drug Effectsen_US
dc.subject.meshAdenosine - Pharmacologyen_US
dc.subject.meshAdenosine Triphosphate - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshElectrophysiologyen_US
dc.subject.meshGlyburide - Pharmacologyen_US
dc.subject.meshGuinea Pigsen_US
dc.subject.meshHeart - Drug Effects - Physiologyen_US
dc.subject.meshHeart Atriaen_US
dc.subject.meshMaleen_US
dc.subject.meshMyocardium - Cytology - Metabolismen_US
dc.subject.meshPotassium Channels - Drug Effects - Physiologyen_US
dc.subject.meshReaction Time - Drug Effectsen_US
dc.titleContribution of ATP-sensitive potassium channels to the electrophysiological effects of adenosine in guinea-pig atrial cellsen_US
dc.typeArticleen_US
dc.identifier.emailLi, GR:grli@hkucc.hku.hken_US
dc.identifier.authorityLi, GR=rp00476en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid7623281-
dc.identifier.scopuseid_2-s2.0-0029043615en_US
dc.identifier.volume484en_US
dc.identifier.issue3en_US
dc.identifier.spage629en_US
dc.identifier.epage642en_US
dc.identifier.isiWOS:A1995QX93000009-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridLi, GR=7408462932en_US
dc.identifier.scopusauthoridFeng, J=7403884361en_US
dc.identifier.scopusauthoridShrier, A=7005657095en_US
dc.identifier.scopusauthoridNattel, S=36048738800en_US

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats