Somatosensory inhibition of vagal baroreflex bradycardia: afferent nervous mechanisms

Abstract

Sensory receptors, afferent fibers, and spinal ascending pathways involved in somatosensory inhibition of baroreflex vagal bradycardia (BVB) were studied in chloralose-urethan-anesthetized rats. BVB was induced by electrical stimulation of the aortic depressor nerve (ADN). Among mechanical and thermal stimuli applied on a hindlimb, hot water (55 degrees C) immersion was most effective to inhibit BVB. Static hindlimb muscle contraction by ventral root stimulation also produced BVB inhibition that was abolished by muscle relaxation. These findings suggest that thermal nociceptors and muscle receptors, probably chemoreceptors, trigger BVB inhibition when activated. Furthermore, afferent fiber groups responsible for BVB inhibition due to sciatic nerve (ScN) or sural nerve (SU) stimulation were determined. BVB was largely inhibited by activation of A delta-fibers of the ScN or SU, but C-fiber contribution to BVB inhibition was also ascertained by means of selective C-fiber activation. Finally, courses of spinal pathways mediating ScN inhibition of BVB were localized as follows. First, ADN-vagal baroreflex arc of one side was interrupted by unilateral vagotomy. Then ScN inhibition of BVB provoked by the remaining reflex arc was analyzed after spinal cord hemisection at C1 and subsequent lesioning of the cord on the nonsectioned side. Regardless of whether the spinal cord was hemisectioned on any side with respect to the target reflex arc, stimulation of the ScN of either side still inhibited BVB, unless the lateral funiculus of nonsectioned side was extensively lesioned. In conclusion, the spinal BVB-inhibitory pathways are multifold, projecting to bilateral baroreflex vagal centers by crossing the midline at spinal or/and medullary levels.