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 assessed in duodenum, mesentery and skin by increased microvascular permeability using extravasation of Evans blue dye (20mg/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.