Dorsal horn administration of L-arginine accentuates the pressor response evoked by activation of muscle mechanoreceptors.

Recent work from our laboratory suggests that nitric oxide production in the dorsal horn has a modulatory influence on the pressor reflex evoked by static contraction of skeletal muscle. In this study, we tested the hypothesis that nitric oxide production in the dorsal horn is involved in producing the pressor reflex elicited by activation of skeletal muscle mechanoreceptors. Cats were anesthetized with alpha-chloralose (80 mg/kg) and urethane (100 mg/kg) and a laminectomy was performed. With the exception of the L7 dorsal root, the dorsal and ventral roots from L5 to S2 were sectioned on one side. Muscle mechanoreceptors were activated by manually stretching the ipsilateral triceps surae muscle 1.5 cm. To block nitric oxide synthase, a 50 mM solution of nt-nitro-L-argenine methyl ester (L-NAME) (a dose that altered the pressor reflex to static contraction) was microdialyzed into the dorsal horn at L6 and S1. Dialysis of L-NAME failed to attenuate the peak change in mean arterial pressure evoked by muscle stretch (45 +/- 6 mmHg before and 44 +/- 9 mmHg after 2 h of L-NAME dialysis). On the other hand, 2 h of L-arginine dialysis (50 mM) increased the peak pressor response to muscle stretch from 43 +/- 3 to 57 +/- 5 mmHg. These data suggest that administration of L-arginine enhances the excitability of dorsal horn cells receiving input from muscle mechanoreceptors, thus increasing the pressor response evoked by activation of this type of muscle afferent neuron.