Spinal modulation of the muscle pressor reflex by nitric oxide and acetylcholine

Static contraction of skeletal muscle activates the sympathetic nervous system, which in turn increases cardiovascular function. These changes are mediated, in part, by a reflex arising from the contracting muscle. This reflex is termed the exercise pressor reflex or, more simply, the muscle pressor reflex (MPR). Over the past few years, studies have been performed investigating the sensory processing that occurs in the dorsal horn of the spinal cord as it pertains to the MPR. Several putative neurotransmitters and receptors have been implicated in mediating the MPR at the level of the dorsal horn. In addition, several receptor systems have been shown to modulate the MPR at the dorsal horn. We have recently performed studies investigating the potential modulatory role of dorsal horn nitric oxide (NO) and acetylcholine (ACH) on the MPR. Along these lines, our experiments suggest that NO enhances the excitability of dorsal horn cells receiving input from muscle afferent neurons, while ACH decreases the MPR when its concentration in the dorsal horn is elevated. The purpose of this manuscript is to review recently published findings from our laboratory and apply this information in an effort to better understand the integration of sensory input that occurs in the dorsal horn as it pertains to cardiovascular regulation. This review is also designed to stimulate questions as to how these two neurochemicals exert their actions and whether or not they represent or can represent important physiological mechanisms involved in regulating the dorsal horn integration of the MPR.