ObjectiveTo test the hypothesis that nitric oxide is a modulator of ileal water and ion transport. Summary Background DataNitric oxide is produced in the vascular endothelium and enteric neural plexuses of the intestine and is involved in gastrointestinal motility and smooth muscle contractility. Little is known about the role of nitric oxide in intestinal epithelial transport. MethodsTen-centimeter rabbit ileal segments (n = 50) were vascularly perfused with an electrolyte solution containing red cells. The lumen was perfused with a solution containing 14C-PEG. Net fluxes of water and ions were calculated during three 20-minute periods: basal, drug infusion, and recovery. Perfusion pressure was recorded to document changes in vascular resistance. Agents infused included the nitric oxide synthase substrate L-arginine, the nitric oxide source sodium nitroprusside, the substrate control D-arginine, and the nitric oxide synthase inhibitor NG-nitro-Larginine methyl ester.Results L-arginine and sodium nitroprusside caused absorption of water and ions. NG-nitro-L-arginine methyl ester caused secretion of water and ions, which was prevented by synchronous infusion of L-arginine. Infusion of D-arginine had no effect. Both L-arginine and sodium nitroprusside caused mild vasodilation. ConclusionsInhibition of endogenous nitric oxide synthesis by NG-nitro-L-arginine methyl ester causes secretion of water and ions. This secretion is reversed by administration of the nitric oxide synthase substrate L-arginine. These findings are consistent with the hypothesis that endogenous nitric oxide has a proabsorptive influence over the ileum in the basal state.Endothelium-derived relaxing factor, a labile substance formed by endothelial cells, mediates vasodilation and is identical to nitric oxide. 1,2 In addition to its role in vasodilatation, nitric oxide is synthesized in many nonvascular tissues. In platelets, nitric oxide generation from L-arginine acts as a negative feedback on platelet aggregation.3 In neutrophils and macrophages, nitric oxide acts as an effector molecule mediating cytotoxicity.4 In 382 neural tissues, nitric oxide is generated in response to activation of excitatory amino acid receptors, and it activates soluble guanylate cyclase in adjacent nerve terminals.5 The enzyme responsible for nitric oxide synthesis from L-arginine is called nitric oxide synthase. It is convenient to consider the nitric oxide synthases as a family of enzymes, broadly grouped into two classes: constitutive and inducible.6 Nitric oxide synthase is present con-
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