Excitatory amino acid receptors in the caudal ventrolateral medulla mediate a vagal cardiopulmonary reflex in the rat.

The importance of the caudal ventrolateral medulla (CVLM) in mediating vagal cardiopulmonary (Bezold-Jarisch reflex) reflex activity was studied in urethane-anaesthetized rats. Unilateral electrolytic lesion of the CVLM markedly attenuated Bezold-Jarisch reflex responses (hypotension and bradycardia) elicited by intravenous injections of 5-HT. Bilateral lesion of the CVLM virtually abolished the reflex responses. Microinjection of the excitatory amino acid (EAA) receptor antagonist kynurenate (KYN), but not the inactive analogue xanthurenate, into the CVLM markedly attenuated the reflex responses to 5-HT. The N-methyl-D-aspartate (NMDA) receptor antagonist, MK-801 also markedly attenuated reflex activity. Furthermore, lesions, KYN and MK-801 all tended to elevate resting blood pressure and to reduce resting heart rate. These findings support the hypothesis that the CVLM is an important medullary locus mediating cardiovascular reflex integration and that an EAA synapse in the CVLM is important in the cardiopulmonary reflex arc.