Lb. Fernandes et al., RELEASE OF INFLAMMATORY MEDIATORS FROM GUINEA-PIG TRACHEA BY ELECTRICAL-FIELD STIMULATION - LACK OF NEURONAL INVOLVEMENT, The Journal of pharmacology and experimental therapeutics, 270(3), 1994, pp. 1166-1170
Electrical field stimulation (EFS; 5-10 V, 1 ms, 20 Hz for 1 min) of i
solated guinea pig trachea resulted in a rapid increase in tone that i
s blocked by either atropine or tetrodotoxin (TTX). EFS of tracheal sp
irals also caused large increases in the release of certain prostanoid
s with release of prostaglandin (PG)D-2, PGE(2) and PGF(2 alpha) (16.5
-, 3.0- and 4.1-fold, respectively). In contrast to the smooth muscle
response, however, EFS-induced release of prostanoids was not signific
antly altered in the presence of TTX. Removal of the epithelium reduce
d the amount of prostanoids released by EFS. Thus, EFS-induced product
ion of PGD(2), PGE(2) and PGF(2 alpha) was significantly reduced by ab
out 30%, 70% and 80% in epithelium-denuded tissues, respectively. Dire
ct vagal stimulation caused a rapid contraction of the trachealis but
failed to elicit increases in the release of histamine or arachidonic
acid metabolites. Furthermore, the selective stimulant of C-type senso
ry fibers capsaicin (3 mu M) or exogenously applied substance P (1 mu
M) or neurokinin A (1 mu M) failed to induce histamine, leukotriene or
prostanoid release from guinea pig tracheal rings. Although, the mech
anism involved in stimulation of arachidonic acid metabolism by EFS is
unclear, this effect in part involves the epithelium but apparently i
s not mediated by airway elements sensitive to TTX, direct vagal stimu
lation or tachykinins.