Spinal cholinergic inhibition of the pressor response to skeletal muscle activation.
The purpose of this study was to delineate the role of the cholinergic pathway within the spinal cord in the reflex cardiovascular responses to muscle activity. Based on dose-response experiments, we microdialyzed a 0.1 mM solution of the acetylcholinesterase inhibitor neostigmine into the L7 level of the dorsal horn of anesthetized cats to determine its effects on the mean arterial blood pressure (MAP) and heart rate (HR) responses to static muscle contraction or passive stretch. The peak responses to 1-min contractions and stretches were reduced from control levels after 1 h of drug administration. In four experiments, the cardiovascular responses returned to control levels after a 2-h recovery period. Perfusion of the cholinergic receptor antagonist atropine accentuated the peak MAP response to muscle contraction. By contrast, atropine administration had no effect on the peak MAP adjustment to passive muscle stretch. These data support the hypothesis that increased acetylcholine (ACh) concentrations in the spinal cord inhibit the reflex cardiovascular responses to static muscle contraction. Further, the results suggest that the spinal cholinergic system is activated by metabolic changes in skeletal muscle, but likely unaffected by mechanical muscle changes.[1]References
- Spinal cholinergic inhibition of the pressor response to skeletal muscle activation. Hand, G.A., Vrettakos, P.J., Treuhaft, B.S., Shealy, W.D., Wilson, L.B. Brain Res. (1999) [Pubmed]
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