Abstract
It is known that the caudal ventrolateral medulla (CVLM) plays an important role in controlling blood pressure and mediating the cardiovascular effects of centrally acting antihypertensive drugs such as clonidine. Recently, the effect of clonidine was believed to be related to the functional states of N-methyl-D-aspartate (NMDA) receptors. The present work was designed to observe the interactions between clonidine and NMDA receptor in the CVLM. Unilaterally injected clonidine (6 nmol) into the CVLM not only produced a pressor action, but also effectively (P<0.01, n=8) antagonized the decreases in both mean arterial pressure (MAP) (-22.3+/-5.0 to -7.9+/-2.3 mmHg) and heart rate (HR) (-31.9+/-5.9 to -10.3+/-2.7 beats/min) evoked by L-glutamate in the CVLM. Unilaterally injected NMDA receptor antagonist MK801 (200 pmol) into the CVLM significantly increased MAP by 26.5+/-3.7 mmHg and HR by 37.1+/-7.6 beats/min, and completely (P<0.01, n=10) abolished the pressor effect (16.1+/-6.6 to 1.5+/-2.8 mmHg) of clonidine in the CVLM. In conclusion, these findings show that NMDA receptors within the CVLM contribute to clonidine-induced action, and suggest that the CVLM plays an important role in the interaction between clonidine and NMDA receptors.
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