It has been suggested that nitric oxide (NO) influences the actions of L-glutamate and angiotensin II in the brain. In the present study, we examined whether cardiovascular responses to L-glutamate and angiotensin II would be altered in the rostral ventrolateral medulla (RVLM) of rats treated with an NO synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME). Wistar rats were treated with either L-NAME (100 mg/kg/day, n = 9) or vehicle (n = 8) for 4 weeks. L-glutamate (2 nmol/50 nl) or angiotensin II (100 pmol) was then microinjected into unilateral RVLM of anesthetized rats. Upon completion of the experiments, angiotensin-converting enzyme (ACE) activity of the brain stem was measured. The systolic blood pressure after 4 weeks of the treatment was significantly higher in the L-NAME group (203 ± 8 mmHg) than in the control group (142 ± 3 mmHg, p < 0.01). The pressor response to L-glutamate microinjected into the RVLM was significantly greater in the L-NAME group (31 ± 2 mmHg) than in the control group (24 ± 1 mmHg, p < 0.01). Similarly, angiotensin II showed a greater pressor response in the L-NAME group. ACE activity of the brain stem did not differ between the groups. In conclusion, NO may have an inhibitory influence on the actions of L-glutamate and angiotensin II in the RVLM.
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