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(Hypertension. 1997;30:1499-1503.)
© 1997 American Heart Association, Inc.

Articles

Cardiovascular Effects of Nitric Oxide and N-Methyl-D-Aspartate Receptors in the Nucleus Tractus Solitarii of Rats

Wan-Chen Lo; Hui-Ching Lin; Luo-Ping Ger; Che-Se Tung; ; Ching-Jiunn Tseng

From the Department of Medical Education and Research (W.-C.L., L.-P.G., C.-J.T.), Veterans General Hospital–Kaohsiung, Kaohsiung, Taiwan, and the Departments of Pharmacology (H.-C.L., C.-J.T.) and Physiology and Biophysics (C.-S.T.), National Defense Medical Center, Taipei, Taiwan, Republic of China.

Abstract Nitric oxide (NO) is an endogenously synthesized effector molecule that acts as a neurotransmitter with novel properties in both the central and peripheral nervous systems. We previously reported that NO was involved in central cardiovascular regulation and modulated the baroreflex in the nucleus tractus solitarii (NTS) of rats. The aim of the present study was to determine whether NO and excitatory amino acids reciprocally release each other in the NTS. In normotensive Sprague-Dawley rats, intra-NTS microinjection of L-arginine (1 to 100 nmol/60 nL) produced a dose-dependent decrease in blood pressure and heart rate. Microinjection of excitatory amino acids L-glutamate and NMDA also produced depressor and bradycardic effects. These effects of L-glutamate or NMDA were blocked by prior administration of NO synthase inhibitor N^G-methyl-L-arginine or N^G-nitro-L-arginine methyl ester. Similarly, prior administration of N-methyl-D-aspartate (NMDA) receptor antagonist MK-801 and non-NMDA receptor antagonist 6,7-dinitroquinoxaline-2,3-dione significantly attenuated the depressor and bradycardic effect of L-arginine. These results demonstrated a reciprocal attenuation of NO synthase inhibitor and NMDA receptor antagonist on NMDA and L-arginine responses, respectively, in the NTS and suggest that NO and NMDA receptors may interact in central cardiovascular regulation.

Key Words: nitric oxide • N-methylaspartate • L-arginine • solitary nucleus • regulation, cardiovascular • L-NAME

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