Proceedings of The Physiological Society
University of Oxford (2011) Proc Physiol Soc 23, PC16
Diurnal variation in the mechanical and neural components of the baroreflex
C. E. Taylor1, G. Atkinson1, C. K. Willie2, H. Jones1, P. N. Ainslie2, Y. Tzeng3
1. Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, Liverpool, United Kingdom. 2. Department of Human Kinetics, University of British Columbia Okanagan, Kelowna, British Columbia, Canada. 3. Cardiovascular Systems Laboratory, University of Otago, Wellington, New Zealand.
Diminished baroreflex gain is a marker for cardiovascular risk (La Rovere et al., 1988). The incidences of myocardial infarction, sudden cardiac death and stroke are highest between 0600 and 1200h, and yet the mechanisms behind this diurnal variation remain unclear. Our aim was to determine the contribution of the mechanical and neural components of the cardiac baroreflex to diurnal variation in blood pressure (BP) control. Given that diurnal variation has been reported in carotid arterial distensibility (Kool et al., 1991), we hypothesised that time-of-day differences in baroreflex gain are explained by variability in the mechanical component. In 7 men and 5 women (mean ±SD age 24.7 ±4.0 yrs), we measured continuous BP, R-R intervals and carotid artery diameter during intravenous bolus injections of sodium nitroprusside (SNP) followed by phenylephrine (PE) (modified Oxford method) at 0700 and 1600h. The modified Oxford technique quantifies baroreflex gain for falling BP via SNP (G-down) and rising BP via PE (G-up). Integrated gain was determined by plotting beat-to-beat R-R intervals against systolic BP. The mechanical and neural components were calculated from plotting diameter vs systolic BP, and R-R intervals vs carotid artery diameter, respectively. A novel analysis method based on linear mixed models (Atkinson et al., 2010) was employed to compare the integrated, mechanical and neural gains between 0700 and 1600h. An attenuated (P<0.05) baroreflex gain was found in the morning ([mean ± SE] G-up = 13.0 ± 0.6; G-down = 6.3 ± 0.4 ms/mm Hg) compared with the afternoon (G-up = 15.1 ± 0.6; G-down = 12.6 ± 0.4 ms/mm Hg). For rising pressures, the reduced integrated gain in the morning was explained by a smaller (P=0.004) mechanical gain (0.015 ± 0.001mm/mmHg) compared with the afternoon (0.018 ± 0.001mm/mm Hg). However, the reduced falling pressure was explained by a diminished (P<0.0005) neural gain in the morning (256.0 ± 30.6 ms/mm) compared with the afternoon (494.9 ± 48.8 ms/mm). Our findings explicate the underlying mechanisms of diurnal variation in BP control. We suggest that the high prevalence of cardiovascular events in the morning is due to diminished mechanical transduction of pressure into arterial distension at this time. Physical activity and pharmacological interventions targeting the enhancement of barosensory vessel compliance and distensibility may improve the mechanical component of the cardiac baroreflex response, thus reducing the risk of cardiovascular events following waking.
Where applicable, experiments conform with Society ethical requirements