Role of sensory neuropeptides in post‐allergic propranolol‐induced bronchoconstriction in guinea pigs in vivo

Abstract

We conclude that neuropeptides such as neurokinin A and substance P do not directly contribute to the development of PIB after allergic reaction.

Influence of alpha‐adrenoceptor blockade on antigen‐ and propranolol‐induced bronchoconstriction in guinea‐pigs in vivo

“…4). These results indicate that blockade of alpha‐adrenoceptors results in functional bronchodilation or bronchoprotection, but has no effect on the release of chemical mediators, which is an important mechanism of development of PIB after allergic reaction in our guinea‐pig model ( Songür et al , 1994 ; Songür et al , 1995 ; Fujimura et al , 1996a ; Fujimura et al , 1996b ; Fujimura et al , 1996c ). In addition, it is likely that airway allergic reaction may lead to alpha‐adrenoceptor dysfunction as well as beta‐adrenoceptor dysfunction ( Fujimura, Mizuhashi, Ishiura, Myou & Matsuda, 1999).…”

“…Histamine has been shown to be involved in PIB in asthmatic patients ( Abraham et al , 1991 ). Recently, we succeeded in developing an animal model for PIB and revealed that inflammatory mediators contribute to the development of PIB ( Songür et al , 1994 ; Songür, Fujimura, Mizuhashi, Saito & Matsuda, 1995; Fujimura et al , 1996a ; Fujimura, Tsujiura, Songür, Myou & Matsuda, 1996b; Fujimura, Tsujiura, Myou, Ishiura & Matsuda, 1996c). However, the role of alpha‐receptor‐mediated adrenergic nerve activity in this response remains uncertain.…”

A guinea-pig model of ultrasonically nebulized distilled water-induced bronchoconstriction

“…Our previous study confirmed the lack of effect on antigen-induced bronchoconstriction in passively sensitized guinea-pigs (unpublished data), although nebulized furosemide has been shown to inhibit antigen-induced bronchoconstriction [37], but not histamine-or acetylcholine-induced bronchoconstriction [38], our previous study did not show an inhibitory effect of inhaled furosemide on antigen-induced bronchoconstriction in passively sensitized guinea-pigs (unpublished data). It has been postulated that furosemide inhibits cholinergic and excitatory nonadrenergic, noncholinergic neurotransmission [39], but our previous study showed that tachykinin is not involved in antigen-induced bronchoconstriction [40] or propranolol-induced bronchoconstriction after antigen challenge in passively sensitized guinea-pigs [11]. Future studies will be needed to assess the effects of these agents on our guinea-pig model of UNDW-IB.…”

“…As the change in the Pao, but not the absolute value of the Pao, represents the average of changes in the RL and 1/Cdyn when leukotriene C 4 is inhaled [17], we have used ch.anges in the Pao as an overall index of changes in airway calibre when oedema or inflammation of the lung parenchyma is negligible [9][10][11][17][18][19]. UNDW inhalation caused an acute and sharp increase in the Pao in the present study, suggesting the presence of bronchoconstriction but not airway oedema.…”

“…We previously reported a guinea-pig model of propranolol-induced bronchoconstriction [9], in which the inhalation of propranolol 20 min after antigen inhalation caused bronchoconstriction in passively sensitized guinea-pigs. Since specific inhibitors of thromboxane A 2 (TxA 2 ) [9] and platelet-activating factor (PAF) [10], but not sensory neuropeptides [11], significantly inhibited the propranolol-induced bronchoconstriction, we postulated that an allergic mediator mechanism was important in propranolol-induced bronchoconstriction.…”