Gut · 1997
Enhanced mucosal permeability and nitric oxide synthase activity in jejunum of mast cell deficient mice.
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Komatsu S, Grisham M B, Russell J M, Granger D N
Аннотация
BACKGROUND: Recent reports have described a modulating influence of nitric oxide (NO) on intestinal mucosal permeability and have implicated a role for mast cells in this NO mediated process.
AIMS: To assess further the contribution of mast cells to the mucosal permeability changes elicited by the NO synthase (NOS) inhibitor NG-nitro-L-arginine methylester (L-NAME), using mast cell deficient (W/Wv) and mast cell replete mice (+/+).
METHODS: Chromium-51 EDTA clearance (from blood to jejunal lumen), jejunal NOS and myeloperoxidase (MPO) activities, and plasma nitrate/nitrite levels were monitored.
RESULTS: The increased EDTA clearance elicited by intraluminal L-NAME in W/Wv mice (4.4-fold) was significantly greater than the response observed in control (+/+) mice (1.8-fold). The exacerbated response in W/Wv mice was greatly attenuated by pretreatment with either dexamethasone (1.3-fold) or the selective inducible NOS inhibitor, aminoguanidine (1.4-fold), and partially attenuated by the mast cell stabiliser, lodoxamide (2.9-fold). Jejunal inducible NOS activity was significantly higher in W/Wv than in +/+ mice, while jejunal MPO was lower in W/Wv mice than in +/+ mice, suggesting that the higher inducible NOS in W/Wv does not result from the recruitment of inflammatory cells into the gut. The higher inducible NOS activity in the jejunum of W/Wv was significantly reduced by dexamethasone treatment.
CONCLUSIONS: Our results suggest that mast cells normally serve to inhibit inducible NOS activity tonically in the gut and that inhibitors of NOS elicit a larger permeability response when this tonic inhibitory influence is released by mast cell depletion.
AIMS: To assess further the contribution of mast cells to the mucosal permeability changes elicited by the NO synthase (NOS) inhibitor NG-nitro-L-arginine methylester (L-NAME), using mast cell deficient (W/Wv) and mast cell replete mice (+/+).
METHODS: Chromium-51 EDTA clearance (from blood to jejunal lumen), jejunal NOS and myeloperoxidase (MPO) activities, and plasma nitrate/nitrite levels were monitored.
RESULTS: The increased EDTA clearance elicited by intraluminal L-NAME in W/Wv mice (4.4-fold) was significantly greater than the response observed in control (+/+) mice (1.8-fold). The exacerbated response in W/Wv mice was greatly attenuated by pretreatment with either dexamethasone (1.3-fold) or the selective inducible NOS inhibitor, aminoguanidine (1.4-fold), and partially attenuated by the mast cell stabiliser, lodoxamide (2.9-fold). Jejunal inducible NOS activity was significantly higher in W/Wv than in +/+ mice, while jejunal MPO was lower in W/Wv mice than in +/+ mice, suggesting that the higher inducible NOS in W/Wv does not result from the recruitment of inflammatory cells into the gut. The higher inducible NOS activity in the jejunum of W/Wv was significantly reduced by dexamethasone treatment.
CONCLUSIONS: Our results suggest that mast cells normally serve to inhibit inducible NOS activity tonically in the gut and that inhibitors of NOS elicit a larger permeability response when this tonic inhibitory influence is released by mast cell depletion.