Proceedings of The Physiological Society

University College Cork (2004) J Physiol 560P, C6



Simms,Annabel ; Paton,Julian F.R; Pickering,Anthony E;

1. Physiology, University of Bristol, Bristol, United Kingdom. 2. Anaesthesia, University of Bristol, Bristol, United Kingdom.

The baroreceptor reflex is a key regulator of arterial blood pressure. Its main effects are mediated by reciprocal modulation of the sympathetic and parasympathetic nervous systems. However, there is some evidence to suggest that these outflows of the baroreflex can be controlled independently (e.g. Pickering et al., 2003). To identify autonomic differences, we tested whether the sympathetic and parasympathetic baroreceptor reflex outflows have comparable arterial pressure thresholds. Studies were performed on male Wistar rats (80g, 4-5 weeks) using the working heart brainstem preparation (Paton, 1996). Rats were deeply anaesthetised with halothane (until loss of withdrawal reflex), transected sub-diaphragmatically, decerebrated precollicularly and perfused retrogradely via the descending aorta with a Ringer's solution plus ficoll (1.25%) at 32oC. Flow through the preparation was computer controlled with a peristaltic pump to alter baseline arterial pressure or by infusion of vasopressin (2-400pM). Baroreceptors were stimulated with pressure pulses. Recordings were made of arterial pressure, heart rate, phrenic nerve and thoracic sympathetic chain (T8-12) activity. Values quoted are mean±SEM. Pressure pulses of approximately 30mmHg for 1 second evoked graded baroreflex-mediated sympathoinhibition. (30-100%) from a wide range of baseline pressures (30-80mmHg). The peak gain of the baroreflex sympathoinhibition was 2.2±0.09%inhibition/mmHg (n=15). However the cardiac component of the baroreflex was only seen clearly with pulses that crossed a higher pressure threshold (70-90mmHg). The cardiac baroreflex gain changed on crossing this threshold from -0.29±0.04 to -1.57±0.24bpm/mmHg (n=15, p<0.0005, paired t-test). Plots of the arterial pressure-baroreflex gain relationship confirmed the cardiac baroreflex is right shifted by approximately 25mmHg compared to the sympathoinhibition. Dual recordings of sympathetic chain and cardiac vagal nerve support this differential pressure responsiveness. To determine whether the difference in cardiac gain is due to the vagus we added a β-blocker (atenolol 0.5-1mg; n=6), which further increased the pressure threshold for the bradycardia by 8-10mmHg, confirming that the parasympathetic component has a higher threshold. We conclude that the sympathetic and cardiac vagal components of the arterial baroreceptor reflex have different pressure sensitivities suggesting a hierarchy of baroreflex autonomic response. It remains to be determined where within the baroreflex arc this difference is generated.

Where applicable, experiments conform with Society ethical requirements