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.

Pressor reflex evoked by static muscle contraction: role of nitric oxide in the dorsal horn.

In this study, we tested the hypothesis that nitric oxide (NO) production in the dorsal horn is involved in producing the pressor reflex elicited by static contraction of skeletal muscle. 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 and static contraction of the ipsilateral triceps surae muscle was evoked by electrically stimulating the peripheral ends of the L7 and S1 ventral roots. Dialysis of the NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME; 50 mmol/l syringe concentration, based upon dose-response data) into the dorsal horn at L6 and S1 failed to attenuate the peak change in mean arterial pressure (MAP) evoked by static contraction (DeltaMAP in mmHg: 57 +/- 5 before and 50 +/- 6 after 2 h of L-NAME). However, this dialysis of L-NAME reduced the magnitude of the initial pressor response as the MAP at 10 s of the contraction fell from 27 +/- 4 to 17 +/- 4 mmHg. On the other hand, 2 h of L-arginine dialysis (50 mmol/l) shifted the curve representing the time course of the pressor response upward and increased the peak pressor response to static contraction from 51 +/- 9 to 68 +/- 9 mmHg. A 2-h dialysis of D-NAME (50 mmol/l), the inactive enantiomer of L-NAME, had no effect on the time course or the peak pressor response (DeltaMAP in mmHg: 78 +/- 12 before and 72 +/- 15 after). These data suggest that NO production in the dorsal horn has a modulatory influence on the pressor reflex evoked by static contraction of skeletal muscle and that increasing the level of NO in the dorsal horn enhances the excitability of dorsal horn cells to muscle afferent input.