Endogenous nitric oxide does not modulate mesenteric mast cell degranulation in rats

The inhibitory effects of endogenous nitric oxide could explain the decreased mesenteric mast cell degranulation after anaphylaxis in genetically hypertensive rats (SHR). SHR and normotensive rats (NT) were sensitized to ovalbumin and challenged 14 days later. Degranulation of mast cells was assesse...

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Bibliographic Details
Published in:Biochemical pharmacology 2003-06, Vol.65 (12), p.2073-2080
Main Authors: Kwasniewski, Fábio H, Tavares de Lima, Wothan, Bakhle, Y.S, Jancar, Sonia
Format: Article
Language:English
Subjects:
Anaphylaxis
Animals
Biological and medical sciences
Capillary Permeability - drug effects
Capillary Permeability - physiology
Cell Degranulation - drug effects
Cell Degranulation - physiology
Enzyme Inhibitors - pharmacology
Mast cells
Mast Cells - drug effects
Mast Cells - physiology
Medical sciences
Mesentery - cytology
Mesentery - drug effects
NG-Nitroarginine Methyl Ester - pharmacology
Nitric oxide
Nitric Oxide - physiology
Rats
Rats, Inbred SHR
Rats, Inbred WKY
Rats, Wistar
Skin - cytology
Spontaneously hypertensive rat
Vascular permeability
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Summary:The inhibitory effects of endogenous nitric oxide could explain the decreased mesenteric mast cell degranulation after anaphylaxis in genetically hypertensive rats (SHR). SHR and normotensive rats (NT) were sensitized to ovalbumin and challenged 14 days later. Degranulation of mast cells was assessed in duodenum, mesentery and skin by increased microvascular permeability using extravasation of Evans blue dye (20 mg/kg, i.v.), and in the mesentery also by light microscopy after staining with toluidine blue. Pretreatment with an inhibitor of nitric oxide synthesis, l-NAME (30 mg/kg, i.v.) did not change dye extravasation after immunological challenge or after compound 48/80 in mesentery of either SHR or NT. PCA was also defective in SHR. Pretreatment with l-NAME did not affect either the defective PCA in SHR or the normal PCA reaction in NT. Our results show that inhibition by endogenous nitric oxide is not the cause of the defective mast cell degranulation in the SHR nor did it modulate degranulation of mesenteric or skin mast cells in NT.
ISSN:0006-2952
1873-2968
DOI:10.1016/S0006-2952(03)00191-6