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Leptin decreases heart rate associated with increased ventricular repolarization via its receptor.
Lin, Yen-Chang; Huang, Jianying; Hileman, Stan; Martin, Karen H; Hull, Robert; Davis, Mary; Yu, Han-Gang.
Afiliación
  • Lin YC; Graduate Institute of Biotechnology, Chinese Culture University, Taipei, Taiwan;
  • Huang J; Center for Cardiovascular and Respiratory Sciences, Department of Physiology and Pharmacology, and.
  • Hileman S; Department of Physiology and Pharmacology, and.
  • Martin KH; Mary Babb Randolph Cancer Center and Department of Neurobiology and Anatomy, Department of Cardiology and Heart Institute of Health Sciences Center, and.
  • Hull R; Heart Institute, West Virginia University, Morgantown, West Virginia.
  • Davis M; Department of Physiology and Pharmacology, and.
  • Yu HG; Center for Cardiovascular and Respiratory Sciences, Department of Physiology and Pharmacology, and hyu@hsc.wvu.edu.
Am J Physiol Heart Circ Physiol ; 309(10): H1731-9, 2015 Nov 15.
Article en En | MEDLINE | ID: mdl-26408544
Leptin has been proposed to modulate cardiac electrical properties via ß-adrenergic receptor activation. The presence of leptin receptors and adipocytes in myocardium raised a question as to whether leptin can directly modulate cardiac electrical properties such as heart rate and QT interval via its receptor. In this work, the role of local direct actions of leptin on heart rate and ventricular repolarization was investigated. We identified the protein expression of leptin receptors at cell surface of sinus node, atrial, and ventricular myocytes isolated from rat heart. Leptin at low doses (0.1-30 µg/kg) decreased resting heart rate; at high doses (150-300 µg/kg), leptin induced a biphasic effect (decrease and then increase) on heart rate. In the presence of high-dose propranolol (30 mg/kg), high-dose leptin only reduced heart rate and sometimes caused sinus pauses and ventricular tachycardia. The leptin-induced inhibition of resting heart rate was fully reversed by leptin antagonist. Leptin also increased heart rate-corrected QT interval (QTc), and leptin antagonist did not. In isolated ventricular myocytes, leptin (0.03-0.3 µg/ml) reversibly increased the action potential duration. These results supported our hypothesis that in addition to indirect pathway via sympathetic tone, leptin can directly decrease heart rate and increase QT interval via its receptor independent of ß-adrenergic receptor stimulation. During inhibition of ß-adrenergic receptor activity, high concentration of leptin in myocardium can cause deep bradycardia, prolonged QT interval, and ventricular arrhythmias.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Nodo Sinoatrial / Potenciales de Acción / Leptina / Miocitos Cardíacos / Receptores de Leptina / Frecuencia Cardíaca / Ventrículos Cardíacos / Miocardio Tipo de estudio: Risk_factors_studies Límite: Animals Idioma: En Revista: Am J Physiol Heart Circ Physiol Asunto de la revista: CARDIOLOGIA / FISIOLOGIA Año: 2015 Tipo del documento: Article Pais de publicación: Estados Unidos
Texto completo
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Imprimir
XML
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Nodo Sinoatrial / Potenciales de Acción / Leptina / Miocitos Cardíacos / Receptores de Leptina / Frecuencia Cardíaca / Ventrículos Cardíacos / Miocardio Tipo de estudio: Risk_factors_studies Límite: Animals Idioma: En Revista: Am J Physiol Heart Circ Physiol Asunto de la revista: CARDIOLOGIA / FISIOLOGIA Año: 2015 Tipo del documento: Article Pais de publicación: Estados Unidos