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Diurnal Amplitudes of Arterial Pressure and Heart Rate Are Dampened in Clock Mutant Mice and Adrenalectomized Mice

Department of Integrative Physiology (H.S., S.C., K.K.), Institute of Health Biosciences, and Department of Clinical Nutrition (E.T.), Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima 770-8503, Japan; and Department of Clock Cell Biology (K.O., N.I.), National Institute of Advanced Industrial Science and Technology, Tsukuba 305-8566, Japan

Address all correspondence and requests for reprints to: Hiroyoshi Sei, M.D., Ph.D., Department of Integrative Physiology, Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima 770-8503, Japan. E-mail: sei{at}basic.med.tokushima-u.ac.jp.

Arterial pressure (AP), heart rate (HR), and cardiovascular diseases, including ischemic heart attack and cerebrovascular accident, show diurnal variation. Evidence that circadian-related genes contribute to cardiovascular control has been accumulated. In this study, we measured the AP and HR of Clock mutant mice on the Jcl/ICR background to determine the role of the Clock gene in cardiovascular function. Mice with mutated Clock genes had a dampened diurnal rhythm of AP and HR, compared with wild-type control mice, and this difference disappeared after adrenalectomy. The diurnal acrophase in both mean arterial pressure and HR was delayed significantly in Clock mutant mice, compared with wild-type mice, and this difference remained after adrenalectomy. Clock mutant mice had a lower concentration of plasma aldosterone, compared with wild-type mice. Our data suggest that the adrenal gland is involved in the diurnal amplitude, but not the acrophase, of AP and HR, and that the function of the Clock gene may be related to the nondipping type of AP elevation.

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