Literature DB >> 20167926

Inotropic response of cardiac ventricular myocytes to beta-adrenergic stimulation with isoproterenol exhibits diurnal variation: involvement of nitric oxide.

Helen E Collins1, Glenn C Rodrigo.   

Abstract

RATIONALE: Although >10% of cardiac gene expression displays diurnal variations, little is known of their impact on excitation-contraction coupling.
OBJECTIVE: To determine whether the time of day affects excitation-contraction coupling in rat ventricles. METHODS AND
RESULTS: Left ventricular myocytes were isolated from rat hearts at 2 opposing time points, corresponding to the animals resting or active periods. Basal contraction and [Ca(2+)](i) was significantly greater in myocytes isolated during the resting versus active periods (cell shortening 12.4+/-0.3 versus 11.0+/-0.2%; P<0.05 and systolic [Ca(2+)](i) 422+/-12 versus 341+/-9 nmol/L; P<0.01. This corresponded to a greater sarcoplasmic reticulum (SR) Ca(2+) load (672+/-20 versus 551+/-13 nmol/L P<0.001). The increase in systolic [Ca(2+)](i) in response to isoproterenol (>3 nmol/L) was also significantly greater in resting versus active period myocytes, reflecting a greater SR Ca(2+) load at this time. This diurnal variation in response of Ca(2+)-homeostasis to isoproterenol translated to a greater incidence of arrhythmic activity in resting period myocytes. Inhibition of neuronal NO synthase during stimulation with isoproterenol, further increased systolic [Ca(2+)](i) and the percentage of arrhythmic myocytes, but this effect was significantly greater in active period versus resting period myocytes. Quantitative RT-PCR analysis revealed a 2.65-fold increase in neuronal NO synthase mRNA levels in active over resting period myocytes (P<0.05).
CONCLUSIONS: The threshold for the development of arrhythmic activity in response to isoproterenol is higher during the active period of the rat. We suggest this reflects a reduction in SR Ca(2+) loading and a diurnal variation in neuronal NO synthase signaling.

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Year:  2010        PMID: 20167926     DOI: 10.1161/CIRCRESAHA.109.213942

Source DB:  PubMed          Journal:  Circ Res        ISSN: 0009-7330            Impact factor:   17.367


  22 in total

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3.  Cardiomyocyte-specific BMAL1 plays critical roles in metabolism, signaling, and maintenance of contractile function of the heart.

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4.  Mitochondrial production of reactive oxygen species contributes to the β-adrenergic stimulation of mouse cardiomycytes.

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8.  Sustained hemodynamic stress disrupts normal circadian rhythms in calcineurin-dependent signaling and protein phosphorylation in the heart.

Authors:  Nita Sachan; Asim Dey; David Rotter; D Bennett Grinsfelder; Pavan K Battiprolu; Devanjan Sikder; Victoria Copeland; Misook Oh; Erik Bush; John M Shelton; James A Bibb; Joseph A Hill; Beverly A Rothermel
Journal:  Circ Res       Date:  2011-01-13       Impact factor: 17.367

9.  Cardiac-specific mutation of Clock alters the quantitative measurements of physical activities without changing behavioral circadian rhythms.

Authors:  Michael L Ko; Liheng Shi; Ju-Yun Tsai; Martin E Young; Nichole Neuendorff; David J Earnest; Gladys Y-P Ko
Journal:  J Biol Rhythms       Date:  2011-10       Impact factor: 3.182

10.  CLOCK-BMAL1 regulates circadian oscillation of ventricular arrhythmias in failing hearts through β1 adrenergic receptor.

Authors:  Zihao Zhou; Jiamin Yuan; Didi Zhu; Yanhong Chen; Zhiyong Qian; Yao Wang; Peibin Ge; Quanpeng Wang; Xiaofeng Hou; Jiangang Zou
Journal:  Am J Transl Res       Date:  2020-10-15       Impact factor: 4.060

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