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Am J Physiol Heart Circ Physiol 295: H59-H68, 2008. First published May 2, 2008; doi:10.1152/ajpheart.00941.2007
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The genetic contribution to heart rate and heart rate variability in quiescent mice

Reuben Howden,1 Eric Liu,1 Laura Miller-DeGraff,1 Heather L. Keener,1 Christopher Walker,1 James A. Clark,1 Page H. Myers,1 D. Clay Rouse,1 Tim Wiltshire,2 and Steven R. Kleeberger1

1Laboratory of Respiratory Biology, Department of Health and Human Services, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina; and 2Genomics Institute of the Novartis Research Foundation, San Diego, California

Submitted 14 August 2007 ; accepted in final form 14 April 2008

Recent studies have suggested a genetic component to heart rate (HR) and HR variability (HRV). However, a systematic examination of the genetic contribution to the variation in HR and HRV has not been performed. This study investigated the genetic contribution to HR and HRV using a wide range of inbred and recombinant inbred (RI) mouse strains. Electrocardiogram data were recorded from 30 strains of inbred mice and 29 RI strains. Significant differences in mean HR and total power (TP) HRV were identified between inbred strains and RI strains. Multiple significant differences within the strain sets in mean low-frequency (LF) and high-frequency (HF) power were also found. No statistically significant concordance was found between strain distribution patterns for HR and HRV phenotypes. Genomewide interval mapping identified a significant quantitative trait locus (QTL) for HR [LOD (likelihood of the odds) score = 3.763] on chromosome 6 [peak at 53.69 megabases (Mb); designated HR 1 (Hr1)]. Suggestive QTLs for TP were found on chromosomes 2, 4, 5, 6, and 14. A suggestive QTL for LF was found on chromosome 16; for HF, we found one significant QTL on chromosome 5 (LOD score = 3.107) [peak at 53.56 Mb; designated HRV-high-frequency 1 (Hrvhf1)] and three suggestive QTLs on chromosomes 2, 11 and 15. In conclusion, the results demonstrate a strong genetic component in the regulation of resting HR and HRV evidenced by the significant differences between strains. A lack of correlation between HR and HRV phenotypes in some inbred strains suggests that different sets of genes control the phenotypes. Furthermore, QTLs were found that will provide important insight to the genetic regulation of HR and HRV at rest.

electrocardiography; autonomic nervous system; ventilation


Address for reprint requests and other correspondence: R. Howden, Lab. of Respiratory Biology, National Inst. of Environmental Health Sciences, 111 T. W. Alexander Dr., Bldg. 101, Rm. E-214, Research Triangle Park, NC 27709 (e-mail: howden{at}niehs.nih.gov)






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