Sympathetic vasodilation in human muscle

Authors


M. J. Joyner, Department of Anesthesiology, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA

Abstract

The idea that there might be sympathetic vasodilator nerves to skeletal muscle is an old concept that fits with the archaic ‘fight or flight’ model of the sympathetic nervous system. Clear evidence for vasodilator nerves to skeletal muscle began to emerge in animals during the 1930s, when stimulation of selected brainstem areas was shown to evoke hypertension, tachycardia and skeletal muscle vasodilation (i.e. the ‘defense reaction’). By the 1940s and 1950s this idea was well established and it was shown in animals that the sympathetic dilator nerves to muscles were cholinergic. During this time, circumstantial evidence began to suggest the existence of sympathetic cholinergic vasodilator fibres in human skeletal muscle. In this context, the well- known forearm vasodilator response to mental stress was shown to be atropine-sensitive, and absent after surgical sympathectomy. However, while there was clear histological evidence for sympathetic cholinergic dilator fibres in animal muscle, such evidence was not seen in humans. Additionally, attempts to record from sympathetic dilator fibres human muscle have never demonstrated clear evidence for dilator nerve traffic, and many ‘sympathetic dilator’ responses are still present after local anaesthetic nerve block. More recently, the skeletal muscle dilator response to sympathoexcitatory manoeuvres in both humans and animals appears to be nitric oxide (NO)-dependent. While there are clearly atropine-sensitive and NO-dependent dilator nerves to skeletal muscles in animals, our current thinking is that most ‘sympathetic dilator’ responses in human muscle are due to adrenaline or local cholinergic mechanisms acting to stimulate NO release from the vascular endothelium.

Ancillary