ArticleThe Journal of physiology2003
Acute exposure to thyroid hormone increases Na+ current and intracellular Ca2+ in cat atrial myocytes.
Article in The Journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Trial
- Unraveling the cardiac consequences of hypothyroidism: a case report of sinus arrest and bradycardia exacerbated by seasonal changes, escitalopram and medication noncompliance.Oxford medical case reports · 2025Article
- Triiodothyronine supplementation in a sheep model of intensive care.Experimental and therapeutic medicine · 2024Article
- Review
- Deficiency of Thyroid Hormone Reduces Voltage-Gated NaInternational journal of molecular sciences · 2022Article
- Identification of atrial-enriched lncRNA Walras linked to cardiomyocyte cytoarchitecture and atrial fibrillation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Pro-Arrhythmic Signaling of Thyroid Hormones and Its Relevance in Subclinical Hyperthyroidism.International journal of molecular sciences · 2020Review
- Hyperthyroidism, but not hypertension, impairs PITX2 expression leading to Wnt-microRNA-ion channel remodeling.PloS one · 2017Article
- Atrial tachyarrhythmias induced by the combined effects of β1/2-adrenergic autoantibodies and thyroid hormone in the rabbit.Journal of cardiovascular translational research · 2014Article
- The arrhythmogenic consequences of increasing late INa in the cardiomyocyte.Cardiovascular research · 2013Review
- Mitochondria-mediated cardioprotection by trimetazidine in rabbit heart failure.Journal of molecular and cellular cardiology · 2013Article
- Thyroid hormone (T3)-induced up-regulation of voltage-activated sodium current in cultured postnatal hippocampal neurons requires secretion of soluble factors from glial cells.Molecular endocrinology (Baltimore, Md.) · 2009Article
- Molecular components underlying nongenomic thyroid hormone signaling in embryonic zebrafish neurons.Neural development · 2009Article
- Sensory neuron sodium current requires nongenomic actions of thyroid hormone during development.Journal of neurophysiology · 2008Article
- Ginsenoside Re suppresses electromechanical alternans in cat and human cardiomyocytes.American journal of physiology. Heart and circulatory physiology · 2008Article
- Signalling mechanisms in contraction-mediated stimulation of intracellular NO production in cat ventricular myocytes.The Journal of physiology · 2007Article
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Authors and funding
6 authors.
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Abstract
Whole-cell recording methods and fluorescence microscopy were used to study the effects of acute exposure to thyroid hormone (T(3)) on cat atrial myocytes. Acute exposure ( approximately 5 min) to 10 nM T(3) significantly increased tetrodotoxin (TTX)-sensitive inward Na(+) current (I(Na)) at voltages between -40 and +20 mV. At maximal I(Na) activation (-40 mV) T(3) increased peak I(Na) by 32 %. T(3) had no effect on the time course of I(Na) decay, voltage dependence of activation, inactivation, or recovery from inactivation. Comparable exposures to reverse T(3) (rT(3)) or T(4) had no effect on I(Na). L-type Ca2+ current was unaffected by acute exposure to T(3). T(3)-induced increases in I(Na) were unaffected by 50 microM nickel, a blocker of T-type Ca2+ current. T(3) significantly increased cell shortening (+62 %) and could elicit spontaneous action potentials arising from Ca2+ -mediated after-depolarizations. T(3) (but not rT(3)) significantly increased baseline intracellular Ca2+, release of Ca2+ from sarcoplasmic reticulum (SR) and caffeine (10 mM)-induced release of SR Ca2+. We conclude that acute T(3) exposure increases Na(+) influx via I(Na) and thereby stimulates reverse-mode Na(+)-Ca2+ exchange to increase intracellular Ca2+ content and release. As a result, T(3) increases contraction strength, and can initiate Ca2+ -mediated arrhythmic activity. Acute non-genomic effects of T(3) can contribute to the positive inotropy and sinus (atrial) tachycardia traditionally attributed to chronic, genomic effects of elevated thyroid hormone on atrial muscle.
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