Abstract

The role of nitric oxide (NO) was determined using a NO synthase inhibitor, N G-nitro-arginine methyl ester ( l.-NAME; 20 mg/kg bolus and 0.05 mg/kg per min) in the renal sympathetic and hypotensive response to systemic anaphylaxis induced by Ascaris suum antigen (10 mg, i.v.) in naturally sensitized anesthetized dogs. Renal nerve activity (RNA) in animals pretreated with D-NAME, the biologically inactive enantiomer ( n = 7), showed an initial increase (192 t 32%, (mean ± SE)) followed by a decrease (61 ± 14%) after antigen. Pretreatment with 1.-NAME ( n = 7) did not affect the initial sympathoexcitation but abolished the secondary sympathoinhibition (110 ± 13%). However, the depressor response to antigen was not different between the l.-NAME and d-NAME groups (−87 ± 13 mmHg and −84 ± 12 mmHg). In conclusion, NO is involved in the anaphylaxis-induced renal sympathoinhibitory response but not hypotension in anesthetized dogs.

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