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1 from COX-1(-/-) mice were hyperresponsive to bronchoconstrictors.
2  causing changes in airway responsiveness to bronchoconstrictors.
3 a(2+)]i, although to a much lower level than bronchoconstrictors.
4       Originally recognized for their potent bronchoconstrictor actions, they were subsequently deter
5 nto the chemotaxin LTB4, which has no direct bronchoconstrictor activity.
6 ffects of reducing [Ca(2+) ](i) responses to bronchoconstrictor agonist via blunted plasma membrane C
7                             Leukotrienes are bronchoconstrictor and vasoactive lipid mediators that a
8 fore, involvement of ADO A3 receptors in the bronchoconstrictor and/or inflammatory effects have to b
9 everses the increase in [Ca(2+)]i induced by bronchoconstrictors, and this lowering of the [Ca(2+)]i
10 of an asthmatic response to several types of bronchoconstrictor challenge.
11            Anti-leukotrienes inhibit several bronchoconstrictor challenges, including allergens, exer
12 high concentrations of inhaled NO reduce the bronchoconstrictor effect of methacholine in animal mode
13 sts that, in addition to the well-known anti-bronchoconstrictor effect, tiotropium might also display
14 he TP receptor to induce proinflammatory and bronchoconstrictor effects.
15 is study was to determine whether the potent bronchoconstrictor endothelin-1 was coupled to the activ
16 istance in response to increasing doses of a bronchoconstrictor following OVA immunization and challe
17          Through secretion of ET-1, a potent bronchoconstrictor, Hic-5 drives epithelial mechanotrans
18                  Adenosine (ADO) is a potent bronchoconstrictor in allergic patients and has been sho
19 ated that Rac1 activation is responsible for bronchoconstrictor-induced increase in intracellular Ca(
20 irway eosinophilia and induce the release of bronchoconstrictor mediators from mast cells such as his
21 ion with increased release of vasoactive and bronchoconstrictor mediators.
22 ed airway resistance response to the inhaled bronchoconstrictor methacholine in the TG mice.
23 aggerated airflow obstruction in response to bronchoconstrictors), mucus overproduction and chronic e
24 ntracellular selective inhibitor of multiple bronchoconstrictor receptors, may play a central role in
25 ase in isolated mast cells, and prevents the bronchoconstrictor response in subjects with exercise-in
26 sponsiveness (BHR) describes the exaggerated bronchoconstrictor response to a host of stimuli such as
27 in E(2) (PGE(2)) inhibits the early and late bronchoconstrictor response to inhaled allergen.
28      Inhaled enoxaparin failed to modify the bronchoconstrictor response to methacholine, and did not
29 cal inhibition of Rac1 in mice prevented the bronchoconstrictor response to methacholine.
30 at treatment with zafirlukast attenuates the bronchoconstrictor response.
31                        Heparin inhibited the bronchoconstrictor responses to exercise by 58%, 78%, an
32                                Moreover, the bronchoconstrictor responses to PGE2 and all other teste
33                                              Bronchoconstrictor responses were recorded from offsprin
34 ncreased sensitivity to direct pharmacologic bronchoconstrictor stimuli, such as inhaled histamine an
35 steinyl leukotrienes and PGD(2) but also the bronchoconstrictor thromboxane A(2) after IgE-dependent
36 ors (a) modulate the activity of cardiac and bronchoconstrictor vagal preganglionic neurones (CVPNs a