Chen Shuang, Ma Shengxing
Department of Obstetrics and Gynecology, University of California, Los Angeles School of Medicine, Harbor-UCLA Medical Center, 1124 W Carson Street, RB-1, Torrance, CA 90502, USA.
Brain Res. 2002 Dec 27;958(2):330-7. doi: 10.1016/s0006-8993(02)03664-8.
The purpose of these studies was to determine the role of gracile nucleus (Gr) and the effects of L-arginine-derived nitric oxide (NO) synthesis in the nucleus on the cardiovascular responses to somatosympathetic reflexes (SSR). Electrical stimulation of sural and tibial nerve to evoke excitatory and inhibitory SSR was carried out in anesthetized Sprague-Dawley rats. Arterial blood pressure and heart rate were monitored during stimulus-evoked SSR following microinjections of the agents into Gr. Cardiovascular responses to electrical stimulation of the sural and tibial nerves were blocked by microinjection of lidocaine into Gr. The hypertensive and tachycardiac responses to stimulation of the sural nerve were attenuated by bilateral microinjection of L-arginine into Gr, but enhanced by the presence of nNOS antisense oligodeoxynucleotides (oligos) in the area. Microinjection of L-arginine into Gr facilitated the hypotensive and bradycardic responses to stimulation of the tibial nerve while pretreatment with nNOS antisense oligos into Gr attenuated the tibial stimulation evoked inhibitory SSR. The stimulus-evoked responses were not altered by microinjection of nNOS sense oligos into Gr. The results show that the cardiovascular responses to stimulus-evoked SSR were inhibited by the presence of a blockade of neuronal conduction in the Gr. L-Arginine-derived NO synthesis in the Gr attenuates the cardiovascular responses to stimulus-evoked excitatory SSR and facilitates the responses to inhibitory SSR. We conclude that NO in the Gr plays an inhibitory role in the central cardiovascular control through SSR regulation.
