Effects of endogenous nitric oxide in activation of group IV muscle afferents

Based on previous observations that acute hypoxemia, which enhances nitric oxide (NO) production, depresses the activation of group IV afferents after repetitive low-frequency muscle stimulation (MS), we hypothesized that endogenous NO modulates the response of these nerve endings to their specific stimuli. The present study in rabbits examined the effects of a blocker of NO synthase (NG-nitro-L-arginine methyl ester L, L-NAME) and an exogenous NO donor (3-morpholinosydnonimine, SIN-1) on the group IV afferents of tibialis anterior. The efficacy of the two test agents was judged by their effects on systemic blood pressure. L-NAME markedly elevated (+46%) the resting discharge rate of group IV afferents but abolished their activation after repetitive MS. After SIN-1 injection, there was a transient decrease in blood pressure, which correlated well with a lowered resting discharge rate of group IV afferents. SIN-1 infusion caused a stable reduction of blood pressure; the resting afferent nerve discharge rate began first to decrease but then recovered control mean values. SIN-1 infusion abolished the activation of group IV afferents after MS. This study indicates that endogenous NO production in a resting or contracting muscle attenuates the baseline activity of group IV muscle afferents and their activation after repetitive muscle contractions.