Proceedings of The Physiological Society

University College Cork (2004) J Physiol 560P, PC2

Communications

NOCTURNAL RESETTING OF THE CAROTID BAROREFLEX - A MECHANISM FOR PROMOTING HYPERTENSION

Cooper,Victoria Louise; Pearson,Stanley ; Bowker,Claire ; Elliott,Mark ; Hainsworth,Roger ;

1. Institute for Cardiovascular Research, University of Leeds, Leeds, United Kingdom. 2. Department of Respiratory Medicine, Leeds Teaching Hospitals, Leeds, United Kingdom.


  • Table 1.

    Baroreflex 'set point' (mmHg)

Obstructive sleep apnoea (OSA) is associated with an increased risk of hypertension, but the reasons for this are unclear. We hypothesise that in normal sleep, as arterial pressure decreases, baroreceptors may reset towards lower pressures and thus protect against hypertension. In OSA however, obstructive episodes result in large increases in arterial pressure which would prevent the downward resetting and could have the opposite effect of resetting baroreceptors towards higher pressures,thus promoting hypertension. We studied 7 healthy control subjects and 14 patients with OSA. The patients were divided into 2 groups, based on 5 separate blood pressure readings, into normotensive (NT, n=7) and hypertensive (HT, n=7). Baroreceptor testing was performed at 9am and 12pm. We used the neck chamber technique to increase and decrease carotid sinus transmural pressure between -40 and 60mmHg. The responses of mean arterial pressure were assessed. Stimulus-response curves were constructed by fitting a sigmoid function to the data. The maximal differential of this curve (equivalent to sensitivity) and corresponding carotid sinus pressure (equivalent to 'set point') were calculated. Baroreflex sensitivity was not different between the 3 groups and did not change significantly with time. In the control group 'set point' was significantly lower at 9am compared to 12pm. However, in both patient groups 'set point' was significantly higher at 9am (Table 1.). At both 9am and 12pm 'setpoint' was significantly higher in HT compared to both controls (P<0.001) and NT (P<0.05). Controls and NT were not different at either timepoint. The results of this study do suggest that in controls there is a downward resetting of the baroreflex in the morning, which may aid in preventing hypertension. The morning upward resetting of the baroreflex in both patient groups may partly explain the development of hypertension in the HT group and may predispose to hypertension in the NT group.

Where applicable, experiments conform with Society ethical requirements