Reciprocal regulation of nitric oxide and glutamate in the nucleus tractussolitarii of rats

Nitric oxide (NO) and glutamate are both important mediators of the central cardiovascular regulation in the nucleus tractus solitarii. Our previous s tudies revealed that the central cardiovascular effects of NO in the nucleu s tractus solitarii could be inhibited by glutamate receptor blockade. On t he other hand, nitric oxide synthase (NOS) inhibitor attenuated the cardiov ascular effects of glutamate. Thus, NO and glutamatergic systems appear to interact in central cardiovascular regulation. The present study examined w hether NO and glutamate may affect each other's release/production in the n ucleus tractus solitarii. A microdialysis probe was implanted into the nucl eus tractus solitarii of male Sprague-Dawley rats, and the changes in the e xtracellular levels of glutamate and NO were determined by high performance liquid chromatography coupled with electrochemical detection and an NO ana lyzer, respectively. The results showed that NO solution elicited > 10 fold increases in the extracellular level of glutamate, which returned to norma l 60 min after the end of NO perfusion. The NO donor N-acetyl-penicillamine (SNAP) had an effect similar to NO solution. Furthermore, the glutamate le vel was reduced to 61% of basal value by perfusion with the NOS inhibitor, N-G-monomethyl-L-arginine (L-NMMA). When glutamate receptor agonist N-methy l-D-aspartic acid (NMDA) or alpha -amino-3-hydroxy-5-methylixoxazole-3-prop ionic acid (AMPA) was administered into the nucleus tractus solitarii, the extracellular NO level was increased by 70-100%, whereas glutamate receptor antagonists (MK-801 hydrogen maleate and 6-cyano-7-nitroquinoxaline-2,3-di one (CNQX)) did not alter the basal levels of NO. These results suggest tha t NO and glutamate may enhance each other's release/production in the nucle us tractus solitarii. This reciprocal regulation of NO and glutamate may he important in central cardiovascular control in the nucleus tractus solitar ii. (C) 2000 Elsevier Science B.V. All rights reserved.