Increased sodium/calcium exchanger activity enhances beta-adrenergic-mediated increase in heart rate: Whole-heart study in a homozygous sodium/calcium exchanger overexpressor mouse model

Heart Rhythm : the Official Journal of the Heart Rhythm Society
Sven KaeseLars Eckardt

Abstract

The cardiac sodium/calcium (Na+/Ca2+) exchanger (NCX) contributes to diastolic depolarization in cardiac pacemaker cells. Increased NCX activity has been found in heart failure and atrial fibrillation. The influence of increased NCX activity on resting heart rate, beta-adrenergic-mediated increase in heart rate, and cardiac conduction properties is unknown. The purpose of this study was to investigate the influence of NCX overexpression in a homozygous transgenic whole-heart mouse model (NCX-OE) on sinus and AV nodal function. Langendorff-perfused, beating whole hearts of NCX-OE and the corresponding wild-type (WT) were studied ± isoproterenol (ISO; 0.2 μM). Epicardial ECG, AV nodal Wenckebach cycle length (AVN-WCL), and retrograde AVN-WCL were obtained. At baseline, basal heart rate was unaltered between NCX-OE and WT (WT: cycle length [CL] 177.6 ± 40.0 ms, no. of hearts [n] = 20; NCX-OE: CL 185.9 ± 30.5 ms, n = 18; P = .21). In the presence of ISO, NCX-OE exhibited a significantly higher heart rate compared to WT (WT: CL 133.4 ± 13.4 ms, n = 20; NCX-OE: CL 117.7 ± 14.2 ms, n = 18; P <.001). ISO led to a significant shortening of the anterograde and retrograde AVN-WCL without differences between NCX-OE and WT. This study is th...Continue Reading

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Citations

Nov 23, 2019·Annual Review of Physiology·Colin H PetersCatherine Proenza
May 16, 2020·Frontiers in Pharmacology·Zsófia KohajdaNorbert Nagy
Oct 18, 2018·Frontiers in Cellular and Infection Microbiology·Martha Valle-SolisMario A Rodríguez
Apr 25, 2019·The Journal of Experimental Biology·Matthew J H GilbertAnthony P Farrell
Jan 15, 2021·The Journal of Pharmacology and Experimental Therapeutics·Yukitoshi IzumiCharles F Zorumski
Feb 20, 2021·The Journal of Pharmacology and Experimental Therapeutics·Michel PelatFrédérique Chézalviel-Guilbert

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