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Article: Electrophysiological mechanisms by which hypothyroidism delays repolarization in guinea pig hearts

TitleElectrophysiological mechanisms by which hypothyroidism delays repolarization in guinea pig hearts
Authors
Issue Date1999
PublisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpheart.physiology.org/
Citation
American Journal Of Physiology - Heart And Circulatory Physiology, 1999, v. 277 n. 1 46-1, p. H211-H220 How to Cite?
AbstractThyroid hormone is known to exert important effects on cardiac repolarization, but the underlying mechanisms are poorly understood. We investigated the electrophysiological mechanisms of differences in repolarization between control guinea pigs and hypothyroid animals (thyroidectomy plus 5-propyl-2-thiouracil). Hypothyroidism significantly prolonged the rate-corrected Q-T interval in vivo and action potential duration (APD) of isolated ventricular myocytes. Whole cell voltage-clamp studies showed no change in current density or kinetics of L-type Ca2+ current, inward rectifier K+ current, or Na+ current in hypothyroid hearts. Dofetilide-resistant current (I(Ks)) step current densities were smaller by ~65%, and tail current densities were reduced by 80% in myocytes from hypothyroid animals compared with controls. The ratio of delayed rectifier step current at +50 mV to tail current at -40 mV was significantly larger in hypothyroid cells for test pulses from 60- to 4,200-ms duration, reflecting a smaller I(Ks). Dofetilide-sensitive current (I(Kr)) densities were not significantly changed. I(Ks) half-activation voltage shifted to more positive voltages in hypothyroidism (29.5 ± 2.2 vs. 21.3 ± 2.7 mV in control, P < 0.01), whereas I(Kr) voltage dependence was unchanged. We conclude that hypothyroidism delays repolarization in the guinea pig ventricle by decreasing I(Ks), a novel and potentially important mechanism for thyroid regulation of cardiac electrophysiology.
Persistent Identifierhttp://hdl.handle.net/10722/162308
ISSN
2015 Impact Factor: 3.324
2015 SCImago Journal Rankings: 1.823
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorBosch, RFen_US
dc.contributor.authorWang, Zen_US
dc.contributor.authorLi, GRen_US
dc.contributor.authorNattel, Sen_US
dc.date.accessioned2012-09-05T05:18:51Z-
dc.date.available2012-09-05T05:18:51Z-
dc.date.issued1999en_US
dc.identifier.citationAmerican Journal Of Physiology - Heart And Circulatory Physiology, 1999, v. 277 n. 1 46-1, p. H211-H220en_US
dc.identifier.issn0363-6135en_US
dc.identifier.urihttp://hdl.handle.net/10722/162308-
dc.description.abstractThyroid hormone is known to exert important effects on cardiac repolarization, but the underlying mechanisms are poorly understood. We investigated the electrophysiological mechanisms of differences in repolarization between control guinea pigs and hypothyroid animals (thyroidectomy plus 5-propyl-2-thiouracil). Hypothyroidism significantly prolonged the rate-corrected Q-T interval in vivo and action potential duration (APD) of isolated ventricular myocytes. Whole cell voltage-clamp studies showed no change in current density or kinetics of L-type Ca2+ current, inward rectifier K+ current, or Na+ current in hypothyroid hearts. Dofetilide-resistant current (I(Ks)) step current densities were smaller by ~65%, and tail current densities were reduced by 80% in myocytes from hypothyroid animals compared with controls. The ratio of delayed rectifier step current at +50 mV to tail current at -40 mV was significantly larger in hypothyroid cells for test pulses from 60- to 4,200-ms duration, reflecting a smaller I(Ks). Dofetilide-sensitive current (I(Kr)) densities were not significantly changed. I(Ks) half-activation voltage shifted to more positive voltages in hypothyroidism (29.5 ± 2.2 vs. 21.3 ± 2.7 mV in control, P < 0.01), whereas I(Kr) voltage dependence was unchanged. We conclude that hypothyroidism delays repolarization in the guinea pig ventricle by decreasing I(Ks), a novel and potentially important mechanism for thyroid regulation of cardiac electrophysiology.en_US
dc.languageengen_US
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpheart.physiology.org/en_US
dc.relation.ispartofAmerican Journal of Physiology - Heart and Circulatory Physiologyen_US
dc.subject.meshAction Potentialsen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCalcium - Metabolismen_US
dc.subject.meshElectrophysiologyen_US
dc.subject.meshGuinea Pigsen_US
dc.subject.meshHeart - Physiologyen_US
dc.subject.meshHypothyroidism - Physiopathologyen_US
dc.subject.meshKineticsen_US
dc.subject.meshMaleen_US
dc.subject.meshPotassium - Metabolismen_US
dc.subject.meshSodium - Metabolismen_US
dc.titleElectrophysiological mechanisms by which hypothyroidism delays repolarization in guinea pig heartsen_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.pmid10409199-
dc.identifier.scopuseid_2-s2.0-0032866458en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0032866458&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume277en_US
dc.identifier.issue1 46-1en_US
dc.identifier.spageH211en_US
dc.identifier.epageH220en_US
dc.identifier.isiWOS:000081442000026-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridBosch, RF=7102263519en_US
dc.identifier.scopusauthoridWang, Z=7410039597en_US
dc.identifier.scopusauthoridLi, GR=7408462932en_US
dc.identifier.scopusauthoridNattel, S=36048738800en_US

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