Vanilloid receptor TRPV1, sensory C-fibers, and activation of adventitial mast cells. A novel mechanism involved in adventitial inflammation

• Published in: Medical hypotheses 2008, Vol.71 (1), p.102-103
• Main Authors: Hu, Cheng Lin, Xiang, Ji Zhou, Hu, Fei Fei
• Format: Article
• Language: English
• Subjects: Animals; Connective Tissue - innervation; Connective Tissue - pathology; Connective Tissue - physiopathology; Humans; Mast Cells - physiology; Models, Biological; Nerve Fibers, Unmyelinated - physiology; Neurogenic Inflammation - etiology; Neurogenic Inflammation - pathology; Neurogenic Inflammation - physiopathology; Substance P - physiology; TRPV Cation Channels - physiology
• ISSN: 0306-9877
• DOI: 10.1016/j.mehy.2008.01.027

The immunological mechanisms on adventitial inflammation has received much attention, while the contribution of nerves to adventitial inflammation has largely been ignored. Although the mechanism of initial chemotaxis of the adventitial inflammatory cells remains unknown, vascular nerves were frequently found in the inflammatory lesions of coronary adventitia and adventitial mast cells connect with sensory nerve fibers in atherosclerotic coronary arteries. The sensory nerves in contact with adventitial mast cells contained the neuropeptides SP and CGRP. These neuropeptides play an important role in the amplification of tissue injury by the increase of both vascular permeability and neutrophil recruitment, and the term ''neurogenic inflammation'' has been coined. Activation of adventitial mast cells, with ensuing release of vasoactive compounds, may cause vasoconstriction in atherosclerotic coronary segments. Therefore, we hypothesize that adventitial vanilloid receptor TRPV1 and sensory C-fibers may play a pistol role for adventitial inflammation.