1988
DOI: 10.1164/ajrccm/137.6.1330
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Abstract: Recent evidence suggests that activation of airway C-fibers, besides causing afferent transmission, also causes release of transmitters from peripheral endings, probably via local axon reflexes, resulting in effects on vascular and bronchial smooth muscle, i.e., vasodilatation, increase in vascular permeability, and bronchoconstriction. In the present study, the release of tachykinins was investigated in the perfused guinea pig lung by various ways of neuronal activation. Substance-P-like immunoreactivity (SP-… Show more

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Cited by 390 publications
(186 citation statements)
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“…Indeed, in a previous study we demonstrated that BK administered directly into the airway lumen caused bronchoconstriction, which appeared to be largely mediated via a cholinergic mechanism and by the release of sensory neuropeptides; both atropine and neuropeptide depletion by capsaicin reduced the BK-induced bronchoconstriction, and the combination of these two pretreatments virtually abolished the effect of BK (Ichinose et al, 1990). Furthermore, BK is capable of releasing tachykinins from sensory nerve endings in guinea-pig perfused lung (Saria et al, 1988). Both ACE and NEP inhibitors potentiate SPinduced bronchoconstriction in vitro (Sekizawa et al, 1987a,b) and in vivo (Shore et al, 1988), presumably by preventing the degradation of SP.…”
Section: Discussionmentioning
confidence: 99%
“…Indeed, in a previous study we demonstrated that BK administered directly into the airway lumen caused bronchoconstriction, which appeared to be largely mediated via a cholinergic mechanism and by the release of sensory neuropeptides; both atropine and neuropeptide depletion by capsaicin reduced the BK-induced bronchoconstriction, and the combination of these two pretreatments virtually abolished the effect of BK (Ichinose et al, 1990). Furthermore, BK is capable of releasing tachykinins from sensory nerve endings in guinea-pig perfused lung (Saria et al, 1988). Both ACE and NEP inhibitors potentiate SPinduced bronchoconstriction in vitro (Sekizawa et al, 1987a,b) and in vivo (Shore et al, 1988), presumably by preventing the degradation of SP.…”
Section: Discussionmentioning
confidence: 99%
“…In guinea pigs, a combination of atropine and capsaicin pretreatment largely eliminates the bronchoconstrictor response to instilled bradykinin, indicating that both a cholinergic reflex and release of neuropeptides from sensory nerves play a part (37). In support of this, it has been shown that bradykinin releases tachykinins from perfused guinea pig lung (80).…”
Section: Kinin Receptors Classificationmentioning
confidence: 79%
“…These responses are likely to be mediated via the activation of specific Bj receptors, as [desArg^]-bradykinin was found to have very limited efl"ect in inducing wheal and flare (57). Additionally, kinins may stimulate sensory nerve endings, thus inducing the local release of potent vasoactive peptides such as substance P (SP), neurokinin A (NKA), and calcitonin gene-related peptide (CGRP) (80). In support of this, pretreatment with topical capsaicin, an irritant which is known to elicit neuropeptide depletion in sensory nerves, greatly attenuates skin responses induced by bradykinin in man (18).…”
Section: Kinin Receptors Classificationmentioning
confidence: 99%
See 1 more Smart Citation
“…The histamine-induced sensory nerve activation in the airways is probably mediated via Hl-receptors (Secher et al, 1982;Saria et al, 1988).…”
Section: Discussionmentioning
confidence: 99%