title: The 24 h pattern of arterial pressure in mice is determined mainly by heart rate-driven variation in cardiac output.
abstract: Few studies have systematically investigated whether daily patterns of arterial blood pressure over 24 h are mediated by changes in cardiac output, peripheral resistance, or both. Understanding the hemodynamic mechanisms that determine the 24 h patterns of blood pressure may lead to a better understanding of how such patterns become disturbed in hypertension and influence risk for cardiovascular events. In conscious, unrestrained C57BL/6J mice, we investigated whether the 24 h pattern of arterial blood pressure is determined by variation in cardiac output, systemic vascular resistance, or both and also whether variations in cardiac output are mediated by variations in heart rate and or stroke volume. As expected, arterial pressure and locomotor activity were significantly (P < 0.05) higher during the nighttime period compared with the daytime period when mice are typically sleeping (+12.5 ± 1.0 mmHg, [13%] and +7.7 ± 1.3 activity counts, [254%], respectively). The higher arterial pressure during the nighttime period was mediated by higher cardiac output (+2.6 ± 0.3 mL/min, [26%], P < 0.05) in association with lower peripheral resistance (-1.5 ± 0.3 mmHg/mL/min, [-13%] P < 0.05). The increased cardiac output during the nighttime was mainly mediated by increased heart rate (+80.0 ± 16.5 beats/min, [18%] P < 0.05), as stroke volume increased minimally at night (+1.6 ± 0.5 μL per beat, [6%] P < 0.05). These results indicate that in C57BL/6J mice, the 24 h pattern of blood pressure is hemodynamically mediated primarily by the 24 h pattern of cardiac output which is almost entirely determined by the 24 h pattern of heart rate. These findings suggest that the differences in blood pressure between nighttime and daytime are mainly driven by differences in heart rate which are strongly correlated with differences in locomotor activity.
authors.affiliation: Department of Laboratory Medicine, University of California, San Francisco, San Francisco, California.
authors.forename: Theodore W
authors.initials: TW
authors.lastname: Kurtz
authors.affiliation: Department of Physiology, Wayne State University School of Medicine, Detroit, Michigan.
authors.forename: Heidi L
authors.initials: HL
authors.lastname: Lujan
authors.affiliation: Department of Physiology, Wayne State University School of Medicine, Detroit, Michigan.
authors.forename: Stephen E
authors.initials: SE
authors.lastname: DiCarlo
keywords: 24‐h variability; hemodynamics