Article date: August 1999
By: A H Van Houwelingen, L A Van Der Avoort, D Van Heuven‐Nolsen, A D Kraneveld, F P Nijkamp, in Volume 127, Issue 7, pages 1583-1588
This study investigates the role of tachykinins in a repeated challenge with dinitrobenzene sulphonic acid (DNS) on the tracheal vascular permeability in dinitrofluorobenzene (DNFB)‐sensitized mice.
DNFB‐contact sensitization was followed by an intranasal (i.n.) challenge with DNS. A second challenge with DNS was administered 24 h after the first challenge. To assess changes in tracheal vascular permeability, Evans blue dye accumulation in tracheal tissue was measured.
A repeated challenge with DNS in DNFB‐sensitized mice led to a 2.8 fold increase in tracheal vascular permeability when compared to DNFB‐sensitized and vehicle‐challenged mice or a 2.5 fold increase when compared to DNFB‐sensitized single DNS‐challenged mice (P<0.001, ANOVA).
RP67580 (10−9 mol mouse−1 i.v.) reduced the increased tracheal vascular permeability induced by a second exposure to DNS in DNFB‐sensitized mice completely when injected 15 min before the second challenge (P<0.001, ANOVA).
The increased tracheal vascular permeability response induced by the second exposure to DNS could be mimicked with i.n. application of capsaicin (10−10 mol mouse−1) or substance P (SP) (10−12 mol mouse−1) to DNFB‐sensitized and single DNS‐challenged mice.
These results suggest that both tachykinin NK1 receptors and sensory nerves are involved in the development of vascular hyperpermeability changes found in the trachea of DNFB‐sensitized mice after a repeated DNS‐challenge.
This study investigates the role of tachykinins in a repeated challenge with dinitrobenzene sulphonic acid (DNS) on the tracheal vascular permeability in dinitrofluorobenzene (DNFB)‐sensitized mice.
DNFB‐contact sensitization was followed by an intranasal (i.n.) challenge with DNS. A second challenge with DNS was administered 24 h after the first challenge. To assess changes in tracheal vascular permeability, Evans blue dye accumulation in tracheal tissue was measured.
A repeated challenge with DNS in DNFB‐sensitized mice led to a 2.8 fold increase in tracheal vascular permeability when compared to DNFB‐sensitized and vehicle‐challenged mice or a 2.5 fold increase when compared to DNFB‐sensitized single DNS‐challenged mice (P<0.001, ANOVA).
RP67580 (10−9 mol mouse−1 i.v.) reduced the increased tracheal vascular permeability induced by a second exposure to DNS in DNFB‐sensitized mice completely when injected 15 min before the second challenge (P<0.001, ANOVA).
The increased tracheal vascular permeability response induced by the second exposure to DNS could be mimicked with i.n. application of capsaicin (10−10 mol mouse−1) or substance P (SP) (10−12 mol mouse−1) to DNFB‐sensitized and single DNS‐challenged mice.
These results suggest that both tachykinin NK1 receptors and sensory nerves are involved in the development of vascular hyperpermeability changes found in the trachea of DNFB‐sensitized mice after a repeated DNS‐challenge.
British Journal of Pharmacology (1999) 127, 1583–1588; doi:10.1038/sj.bjp.0702707
DOI: 10.1038/sj.bjp.0702707
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