Glycine increases arterial pressure and augments NMDA-induced pressor responses in the dorsomedial and ventrolateral medulla of cats.

The present study is designed to determine and characterize two neurobiological events. Firstly, we investigated whether increases of systemic arterial pressure (SAP) and sympathetic vertebral nerve activity (VNA) produced by microinjection of glycine (Gly) in the dorsomedial (DM) or rostral ventrolateral medulla (RVLM) are mediated by pressor neurons in DM or RVLM. Secondly, we assessed whether simultaneous microinjections of Gly and N-methyl-D-aspartate (NMDA) in DM or RVLM potentiate the NMDA-pressor effects. Changes in SAP and VNA were recorded in 33 cats under alpha-chloralose and urethane anesthesia. Microinjection of sodium glutamate (Glu, 0.25 M, 30 nl) or Gly (1.0 M, 30 nl) into the DM or RVLM increased SAP and VNA in similar magnitude. Latencies of changes in SAP and VNA induced by Gly, however, were longer (3 s) than those induced by Glu. Prior microinjection of the following antagonists blocked the Gly-induced pressor responses: 2-amino-5-phosphonopentanoate (AP-5, 25 mM, 30 nl), a specific NMDA receptor antagonist; or glutamate diethyl ester (GDEE, 0.5 M, 30 nl), a quisqualate receptor antagonist; or kynurenic acid (KYN, 10 mM, 30 nl), a broad spectrum competitive Glu antagonist. Prior treatment with strychnine (3 mM, 30 nl), a specific Gly antagonist, also blocked the Gly-induced pressor responses. Since Gly is believed to be an inhibitory neurotransmitter, these data suggest that Gly may produce pressor actions via an inhibition on specific inhibitory neurons synapsing with the pressor neurons. NMDA (0.1 M, 30 nl) and Gly (1.0 M, 30 nl) microinjected simultaneously in DM or RVLM produced a greater pressor action than NMDA alone. This potentiation was blocked by KYN, another known antagonist for such potentiation, but was only partially blocked by strychnine.