Inotropic Response of Cardiac Ventricular Myocytes to β-Adrenergic Stimulation With Isoproterenol Exhibits Diurnal Variation

Collins, Helen E.; Rodrigo, Glenn C.

doi:10.1161/circresaha.109.213942

Cited by 44 publications

(51 citation statements)

References 47 publications

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“…S2). There are daily rhythms in sensitivity to catecholamines in different organ systems including the heart, due in part to the down-regulation of adrenergic receptors after stimulation (23,(37)(38)(39). The circadian-mediated rapid rise in epinephrine that we observed at ≈8:00 AM may be particularly problematic in the setting of the concomitant circadian peak in cortisol because cortisol has permissive effects on adrenergic receptors (40).…”

Section: Discussionmentioning

confidence: 83%

Impact of the human circadian system, exercise, and their interaction on cardiovascular function

Scheer

Evoniuk

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

263

248

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The risk of adverse cardiovascular events peaks in the morning (≈9:00 AM) with a secondary peak in the evening (≈8:00 PM) and a trough at night. This pattern is generally believed to be caused by the day/night distribution of behavioral triggers, but it is unknown whether the endogenous circadian system contributes to these daily fluctuations. Thus, we tested the hypotheses that the circadian system modulates autonomic, hemodynamic, and hemostatic risk markers at rest, and that behavioral stressors have different effects when they occur at different internal circadian phases. Twelve healthy adults were each studied in a 240-h forced desynchrony protocol in dim light while standardized rest and exercise periods were uniformly distributed across the circadian cycle. At rest, there were large circadian variations in plasma cortisol (peak-to-trough ≈85% of mean, peaking at a circadian phase corresponding to ≈9:00 AM) and in circulating catecholamines (epinephrine, ≈70%; norepinephrine, ≈35%, peaking during the biological day). At ≈8:00 PM, there was a circadian peak in blood pressure and a trough in cardiac vagal modulation. Sympathetic variables were consistently lowest and vagal markers highest during the biological night. We detected no simple circadian effect on hemostasis, although platelet aggregability had two peaks: at ≈noon and ≈11:00 PM. There was circadian modulation of the cardiovascular reactivity to exercise, with greatest vagal withdrawal at ≈9:00 AM and peaks in catecholamine reactivity at ≈9:00 AM and ≈9:00 PM. Thus, the circadian system modulates numerous cardiovascular risk markers at rest as well as their reactivity to exercise, with resultant profiles that could potentially contribute to the day/night pattern of adverse cardiovascular events.

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Section: Discussionmentioning

confidence: 83%

Impact of the human circadian system, exercise, and their interaction on cardiovascular function

Scheer

Evoniuk

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

263

248

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“…However, it is becoming increasingly clear that cardiovascular components exhibit time-of-day-dependent oscillations in their responsiveness to extrinsic factors, which in turn likely influence outcomes following pathologic events ( e.g. , myocardial infarction) (Collins and Rodrigo 2010; Durgan, et al 2010; Durgan, et al 2006; Durgan, et al 2011b; Durgan and Young 2010; Sachan, et al 2011). Currently, the relative contribution of extrinsic versus intrinsic factors towards rhythms in cardiovascular function and dysfunction remains undefined.…”

Section: Introductionmentioning

confidence: 99%

Cardiomyocyte-Specific BMAL1 Plays Critical Roles in Metabolism, Signaling, and Maintenance of Contractile Function of the Heart

et al. 2014

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Circadian clocks are cell autonomous, transcriptionally-based, molecular mechanisms that confer the selective advantage of anticipation, enabling cells/organs to respond to environmental factors in a temporally appropriate manner. Critical to circadian clock function are two transcription factors, CLOCK and BMAL1. The purpose of the present study was to reveal novel physiologic functions of BMAL1 in the heart, as well as determine the pathologic consequences of chronic disruption of this circadian clock component. In order to address this goal, we generated cardiomyocyte-specific Bmal1 knockout (CBK) mice. Following validation of the CBK model, combined microarray and in silico analyses were performed, identifying 19 putative direct BMAL1 target genes, which included a number of metabolic (e.g., β-hydroxybutyrate dehydrogenase 1 [Bdh1]) and signaling (e.g., the p85α regulatory subunit of phosphatidylinositol 3-kinase [Pik3r1]) genes. Results from subsequent validation studies were consistent with regulation of Bdh1 and Pik3r1 by BMAL1, with predicted impairments in ketone body metabolism and signaling observed in CBK hearts. Furthermore, CBK hearts exhibited depressed glucose utilization, as well as a differential response to a physiologic metabolic stress (i.e., fasting). Consistent with BMAL1 influencing critical functions in the heart, echocardiographic, gravimetric, histologic, and molecular analyses revealed age-onset development of dilated cardiomyopathy in CBK mice, which was associated with a severe reduction in lifespan. Collectively, our studies reveal that BMAL1 influences metabolism, signaling, and contractile function of the heart.

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“…The increase in systolic intracellular calcium in response to isoproterenol was also significantly greater in resting periods than in active periods, reflecting a greater calcium load in the sarcoplasmic reticulum in the resting period. 92 Wild-type hearts but not CCM hearts showed a marked diurnal variation in responsiveness to an elevation in workload ex vivo, with a greater increase in cardiac power and efficiency during the dark (active) phase than in the light (inactive) phase. 93 Qi and Boateng put forward an interesting hypothesis that CLOCK localizes to the sarcomeric z-disk and senses myofilament cross-bridge activity in neonatal cardiomyocytes.…”

Section: Contractilementioning

confidence: 92%

Circadian rhythm and cardiovascular disorders

Zhang¹,

Sabeh²,

Jain³

2014

CPT

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Abstract:Circadian rhythmicity affects all living organisms on earth. Central and peripheral cellular clocks have the ability to oscillate and be entrained to environmental cues, thus allowing organisms to anticipate and synchronize their physiologic processes and behavior to recurring daily environmental alterations. Disruption of the circadian rhythm in modern life, such as by shift work and jet travel, leads to dyssynchrony of the central and peripheral clocks, and is an independent risk factor for cardiovascular disease and the metabolic syndrome. Aging has also been associated with attenuated cellular rhythmicity. Here we summarize the clinical observations linking cardiovascular health to circadian rhythm. In addition, we discuss recent advances in experimental models for understanding the clock machinery in terms of a variety of physiologic processes within the cardiovascular system. Together, these studies build the foundation for applying our knowledge of circadian biology to the development of novel therapy for cardiovascular disorders.

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Inotropic Response of Cardiac Ventricular Myocytes to β-Adrenergic Stimulation With Isoproterenol Exhibits Diurnal Variation

Cited by 44 publications

References 47 publications

Impact of the human circadian system, exercise, and their interaction on cardiovascular function

Impact of the human circadian system, exercise, and their interaction on cardiovascular function

Cardiomyocyte-Specific BMAL1 Plays Critical Roles in Metabolism, Signaling, and Maintenance of Contractile Function of the Heart

Circadian rhythm and cardiovascular disorders

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