Peripheral circadian clock rhythmicity is retained in the absence of adrenergic signaling

Dermot F. Reilly, Anne M. Curtis, Yan Cheng, Elizabeth J. Westgate, Radu D. Rudic, Georgios Paschos, Jacqueline Morris, Ming Ouyang, Steven A. Thomas, Garret A. FitzGerald

Research output: Contribution to journalArticlepeer-review

49 Scopus citations


OBJECTIVE - The incidence of heart attack and stroke undergo diurnal variation. Molecular clocks have been described in the heart and the vasculature; however it is largely unknown how the suprachiasmatic nucleus (SCN) entrains these peripheral oscillators. METHODS AND RESULTS - Norepinephrine and epinephrine, added to aortic smooth muscle cells (ASMCs) in vitro, altered Per1, E4bp4, and dbp expression and altered the observed oscillations in clock gene expression. However, oscillations of Per1, E4bp4, dbp, and Per2 were preserved ex vivo in the aorta, heart, and liver harvested from dopamine β-hydroxylase knockout mice (Dbh) that cannot synthesize either norepinephrine or epinephrine. Furthermore, clock gene oscillations in heart, liver, and white adipose tissue phase shifted identically in Dbh mice and in Dbh controls in response to daytime restriction of feeding. Oscillation of clock genes was similarly preserved ex vivo in tissues from Dbh and Dbh chronically treated with both propranolol and terazosin, thus excluding compensation by dopamine in Dbh mice. CONCLUSIONS - Although adrenergic signaling can influence circadian timing in vitro, peripheral circadian rhythmicity is retained despite its ablation in vivo.

Original languageEnglish (US)
Pages (from-to)121-126
Number of pages6
JournalArteriosclerosis, thrombosis, and vascular biology
Issue number1
StatePublished - Jan 2008
Externally publishedYes


  • Adrenergic
  • Catecholamines
  • Circadian
  • Norepinephrine
  • Sympathetic

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine


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