Activation of NMDA and non-NMDA receptors in the caudal ventrolateral medulla dilates the airways

The caudal ventrolateral medulla (CVLM) participates in the central control of airway caliber. For example, both electrical and chemical stimulation of the CVLM decrease total lung resistance by withdrawing cholinergic input to airway smooth muscle. Although cell bodies in the CVLM have been shown to play an important role in mediating the central control of airway caliber, the pharmacological mechanism in this brainstem region responsible for causing this airway dilation is unknown. We, therefore, examined the role played by ionotropic excitatory amino acid receptors in the CVLM in the control of airway caliber in chloralose-anesthetized dogs. We found that microinjection of 3.9 pmol of NMDA or AMPA or quisqualate into 12 sites in the CVLM decreased total lung resistance by 1.5±0.2 cm H₂O l^-1 s^-1 (p<0.05), and that microinjection of 3.9 pmol of kainic acid into 9 in the CVLM decreased total lung resistance by 0.5±0.1 cm H₂O l^-1 s^-1 (p<0.05). The decrease in total lung resistance evoked by either NMDA or AMPA or quisqualate was not different (p>0.05) while that evoked by kainic acid was significantly smaller. Additionally, microinjection of NMDA or AMPA or quisqualate caused a small but significant decrease in mean arterial pressure and heart rate (p<0.05). These experiments demonstrate that the airway dilation evoked by stimulation of excitatory amino acid receptors in the CVLM is mediated by both NMDA and non-NMDA receptors. Copyright (C) 1998 Elsevier Science B.V.