(Hypertension. 2000;36:195.)
© 2000 American Heart Association, Inc.
Scientific Contributions |
From the Hypertension Research Center (E.J., M.K., A.A.) and the Department of Preventive Medicine and Community Health (J.H.S.), University of Medicine and Dentistry of New Jersey, New Jersey Medical School, Newark; the Department of Epidemiology and Biostatistics (N.J.S.), Case Western Reserve University, Cleveland, Ohio; the Program for Population Genetics and Department of Biostatistics (N.J.S.), Harvard University School of Public Health, Boston, Mass; the Jackson Laboratory (N.J.S., J.H.S.), Bar Harbor, Maine; and the Danish Twin Register (K.O.K.), Genetic Epidemiology Research Unit, Institute of Community Health, Odense University, Denmark.
Correspondence to Abraham Aviv, Room F-464, MSB, Hypertension Research Center, University of Medicine and Dentistry of New Jersey, 185 S Orange Ave, Newark, NJ 07103-2714. E-mail avivab{at}umdnj.edu
AbstractThere is evidence that telomeres, the ends of chromosomes, serve as clocks that pace cellular aging in vitro and in vivo. In industrialized nations, pulse pressure rises with age, and it might serve as a phenotype of biological aging of the vasculature. We therefore conducted a twin study to investigate the relation between telomere length in white blood cells and pulse pressure while simultaneously assessing the role of genetic factors in determining telomere length. We measured by Southern blot analysis the mean length of the terminal restriction fragments (TRF) in white blood cells of 49 twin pairs from the Danish Twin Register and assessed the relations of blood pressure parameters with TRF. TRF length showed an inverse relation with pulse pressure. Both TRF length and pulse pressure were highly familial. We conclude that telomere length, which is under genetic control, might play a role in mechanisms that regulate pulse pressure, including vascular aging.
Key Words: blood pressure pulse age twins
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