Nitric oxide mediates the inhibition by interleukin‐1β of pentagastrin‐stimulated rat gastric acid secretion

Bolus injection of interleukin‐1β (2 μg kg−1, i.v.) inhibited acid secretion induced by intravenous infusion of pentagastrin (8 μg kg−1 h−1) in the continuously perfused stomach of the anaesthetized rat. Administration of interleukin‐1β did not modify mean systemic arterial blood pressure. Pretreatment with NG‐nitro‐l‐arginine methyl ester (l‐NAME, 2 −10 mg kg−1, i.v.), but not dexamethasone (5 mg kg−1, s.c. twice over 16 h), restored the acid secretory responses to pentagastrin. The actions of l‐NAME were reversed by the prior administration of l‐arginine (100 mg kg−1, i.v.), but not by its enantiomer d‐arginine (100 mg kg−1, i.v.). l‐NAME (5 mg kg−1, i.v.) increased blood pressure but this was not the mechanism by which interleukin‐induced acid inhibition was prevented, since similar systemic pressor responses induced by phenylephrine (10 μg kg−1 min−1, i.v.), had no such effect. These findings suggest that interleukin‐induced inhibition of acid responses to pentagastrin involves synthesis of NO from l‐arginine.