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THE INVOLVEMENT OF MAST CELLS IN VASODILATATION DUE TO AXON REFLEXES IN INJURED SKIN
Author(s) -
Kiernan J. A.
Publication year - 1972
Publication title -
quarterly journal of experimental physiology and cognate medical sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0033-5541
DOI - 10.1113/expphysiol.1972.sp002164
Subject(s) - degranulation , axon reflex , antidromic , histamine , axon , reflex , free nerve ending , bradykinin , chemistry , mast cell , autacoid , scratching , neuroscience , microbiology and biotechnology , anatomy , stimulation , biology , medicine , endocrinology , immunology , receptor , materials science , composite material
Immediately subjacent to a scratch damaging the epidermis of the external ear of the albino rat, all the dermal mast cells are degranulated. The proportion of degranulating mast cells is increased from about 43% to about 56% in areas of vasodilatation due to axon reflexes in the skin surrounding such a scratch. A similar degree of degranulation follows antidromic stimulation of the common trunk of the great auricular and lesser occipital nerves. It is shown that the degranulation of mast cells, like the vasodilatation, is mediated by the somatic sensory axons supplying the skin. A theory is advanced in which it is proposed that histamine, released from degranulated mast cells at the site of an injury, stimulates sensory nerve endings initiating an axon reflex. A transmitter substance, possibly adenosine triphosphate, is released from other terminations of the same neuron and causes degranulation of mast cells. Proteolytic enzymes released from these mast cells act upon a substrate present in the extracellular fluid to form bradykinin, which dilates nearby arterioles.