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dc.date.accessioned2017-01-10T11:16:03Z
dc.date.available2017-01-10T11:16:03Z
dc.date.created2016-11-27T13:56:01Z
dc.date.issued2016
dc.identifier.citationBerg, Torill . M-currents (Kv7.2-7.3/KCNQ2-KCNQ3) Are Responsible for Dysfunctional Autonomic Control in Hypertensive Rats. Frontiers in Physiology. 2016, 7 (584)
dc.identifier.urihttp://hdl.handle.net/10852/53496
dc.description.abstractAutonomic dysfunctions play important roles in hypertension, heart failure and arrhythmia, often with a detrimental and fatal effect. The present study analysed if these dysfunctions involved M-channels (members of the Kv7/KNCQ family) spontaneously hypertensive rats (SHR). Cardiac output and heart rate (HR) were recorded by a flow probe on the ascending aorta in anesthetized SHR and normotensive rats (WKY), and blood pressure (BP) by a femoral artery catheter. Total peripheral vascular resistance (TPR) was calculated. XE-991 (Kv7.1-7.4-inhibitor) reduced resting HR in WKY but only after reserpine in SHR. XE-991 increased TPR and BP baseline in both strains. Retigabine (Kv7.2-7.5-opener) reduced HR, TPR and BP, also after reserpine. Depolarization induced by 3,4-diaminopyridine (3,4-DAP), a voltage-sensitive K+ channel (Kv) inhibitor, activated release of both acetylcholine and norepinephrine, thus activating an initial, cholinergic bradycardia in SHR, followed by sustained, norepinephrine-dependant tachycardia in both strains. XE-991 augmented the initial 3,4-DAP-induced bradycardia and eliminated the late tachycardia in SHR, but not in WKY. The increased bradycardia was eliminated by hexamethonium and methoctramine (M2muscarinic receptor antagonist) but not reserpine. Retigabine eliminated the increased bradycardia observed in reserpinized SHR. XE-991 also increased 3,4-DAP-stimulated catecholamine release, but not after hexamethonium or reserpine. Conclusions: M-currents hampered parasympathetic ganglion excitation and, through that, vagal control of HR, in SHR but not WKY. M-currents also opposed catecholamine release in SHR but not in WKY. M-currents represented a vasodilatory component in resting TPR-control, with no strain-related difference detected. Excessive M-currents may represent the underlying cause of autonomic dysfunctions in hypertension.en_US
dc.languageEN
dc.language.isoenen_US
dc.publisherFrontiers Research Foundation
dc.rightsAttribution 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.titleM-currents (Kv7.2-7.3/KCNQ2-KCNQ3) Are Responsible for Dysfunctional Autonomic Control in Hypertensive Ratsen_US
dc.typeJournal articleen_US
dc.creator.authorBerg, Torill
cristin.unitcode185,51,12,50
cristin.unitnameSeksjon for fysiologi
cristin.ispublishedfalse
cristin.fulltextoriginal
cristin.qualitycode1
dc.identifier.cristin1404645
dc.identifier.bibliographiccitationinfo:ofi/fmt:kev:mtx:ctx&ctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=Frontiers in Physiology&rft.volume=7 (584)&rft.spage=&rft.date=2016
dc.identifier.jtitleFrontiers in Physiology
dc.identifier.volume7
dc.identifier.pagecount11
dc.identifier.doihttp://dx.doi.org/10.3389/fphys.2016.00584
dc.identifier.urnURN:NBN:no-56697
dc.type.documentTidsskriftartikkelen_US
dc.type.peerreviewedPeer reviewed
dc.source.issn1664-042X
dc.identifier.fulltextFulltext https://www.duo.uio.no/bitstream/handle/10852/53496/1/fphys-07-00584-berg.pdf
dc.type.versionPublishedVersion
cristin.articleid584


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