Figure 5 Sympathetic influence on vasoregulation, leucocyte extravasation, and dendritic cell exodus. (A) An immune stimulus induces local production of substance P (SP), calcitonin gene related peptide (CGRP), and nitric oxide (NO). Among others, these mediators lead to vasodilation. Norepinephrine (NE) and neuropeptide Y (NPY) counteract vasodilation via α1 adrenergic and NPY Y1 receptors. Chemotactic factors, including SP and NE via β adrenoceptors and sympathetic opioid peptides, support leucocyte extravasation. Elevated concentrations of NE and NPY is indicated by numerous purple dots. Thus neurotransmitters of the sympathetic nervous system support chemotaxis, which is a very early event in the beginning of an inflammatory reaction. In addition, exodus of relatively immature dendritic cells is supported by α1 adrenergic signalling. (B) After leucocytes are encountered in an inflammatory process, they start to produce proinflammatory cytokines and sympathetic nerve repellent factors, which inhibit neurotransmitter release and lead to loss of sympathetic nerve fibres. This development is typical for the early phase of a wound healing process. TNF, tumour necrosis factor; IL, interleukin.