Journal
EXPERIMENTAL LUNG RESEARCH
Volume 38, Issue 5, Pages 233-249Publisher
TAYLOR & FRANCIS INC
DOI: 10.3109/01902148.2012.673050
Keywords
bronchoconstriction; isolated guinea pig lung; tachykinin NK3-receptors; tachykinin NK3-receptor agonist [MePhe(7)]-neurokinin B; vagal stimulation
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The neuromodulatory action of the tachykinin NK3-receptor agonist [MePhe(7)]-neurokinin B ([MePhe(7)]-NKB) was evaluated on vagal stimulation-induced bronchoconstriction in nonsensitized nonchallenged and ovalbumin (OVA)-sensitized and -challenged guinea pig using the isolated perfused lung preparation. Lungs were placed inside a warmed (37 degrees C) glass chamber and suspended from a force displacement transducer (Grass FT-03) with both vagi connected to a stimulating electrode. Isolated lungs were stimulated at a constant voltage (20 V) and pulse duration (5 ms) with electrical stimulation frequencies ranging from 1 to 128 Hz. The authors demonstrated that vagal stimulation produced frequency-dependent bronchoconstriction and [MePhe(7)]-NKB, at a dose (0.1 mu M) that does not produce bronchoconstriction by itself, potentiated the vagally induced bronchoconstriction at all frequencies in nonsensitized nonchallenged animals and to a greater extent in OVA-sensitized and -challenged guinea pigs; the potentiations were totally inhibited by the tachykinin NK3-receptor antagonist SR 142801 (1 mu M). In a second set of experiments, [MePhe(7)]-NKB produced bronchoconstriction in a dose-dependent (1 to 300 mu g/mL) manner with similar potencies and maximum responses in nonsensitized nonchallenged (EC50 = 8.6 +/- 1.1 mu M; E-Max = 61.1 +/- 3.5 mm Hg) and OVA-sensitized and -challenged (EC50 = 8.5 +/- 1.3 mu M; E-Max = 63.5 +/- 3.7 mm Hg) animals. In conclusion, these results demonstrated that [MePhe(7)]-NKB potentiated vagal stimulation-induced bronchoconstriction via the tachykinin NK3-receptors and OVA sensitization caused development of airway hyperresponsiveness in these potentiations. However, OVA sensitization had no effect on airway responsiveness of vagal stimulation-and [MePhe(7)]-NKB-induced bronchoconstrictions.
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