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In patients with fibromyalgia syndrome (FMS) and temporomandibular disorder (TMD), stress and pain may chronically enhance sympathetic activity, altering cardiovascular responses and worsening pain.
When NGF is bound to TrkA, the receptor transmits positive signals that enhance sympathetic neuron growth and survival.
Considering brain injury, cytokines produced in the brain after trauma as well as an increased ICP can enhance sympathetic nerve activity.
The authors suggest that an exposure to prolonged microgravity may enhance sympathetic neural traffic not only to muscle but also to bone.
Spinal reflex pathways not only enhance sympathetic outflow but also α-motoneuron discharge from Onuf's nucleus in the ventrolateral horn of the sacral (S2 S4) spinal cord [ 12].
Noncontractile and necrotic left ventricular segments are known to enhance sympathetic afferent and efferent activity, which is manifested as HRV reduction and eventually leads to greater myocardial vulnerability and electrical instability, as well as to the risk of malignant arrhythmias.
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Even if it is unclear whether myocardial adrenergic stimulation is the only pathophysiological mechanism associated with SRC, enhanced sympathetic tone inducing endogenous catecholamine's stimulation of the myocardium was always reported [3].
Enhanced sympathetic signaling partially compensates for deteriorating myocardial function [ 9].
Another potential contributing factor is enhanced sympathetic activity.
It was also shown that EA stimulation significantly enhanced sympathetic activity [ 34].
Previously, we have reported that GDNF enhanced sympathetic axon growth toward cardiomyocytes [ 8].
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