Comparison of the inhibitory potencies of N(G)-methyl-, N(G)-nitro- and N(G)-amino-L-arginine on EDRF function in the rat: evidence for continuous basal EDRF release.

摘要: The relative potencies of the argininolytic agents NG-methyl-L-arginine (L-NMA), NG-nitro-L-arginine (L-NNA) and NG-amino-L-arginine (L-NAA) were assayed by their inhibitory effect on both basal stimulated release endothelium-derived NO in vitro vivo. Basal was indirectly assessed ability analogs to contract phenylephrine-preconstricted rat aortic rings produce a hypertensive response awake, unanesthetized normotensive rats. In rings, three induced vasocontraction inhibited vasorelaxation mediated ACh-stimulated endothelial release. this latter assay, L-NNA 30 times more potent than either L-NMA or L-NAA. free-moving rats, caused dose-dependent increases arterial pressure due blockade endogenous formation. Dose-response analysis indicated that 87 230 L-NAA, respectively. Pretreatment with also found selectively inhibit, but not abolish, depressor effects acetylcholine phenylephrine- vasopressin-infused normotensive-pithed These studies indicate is antagonist relaxing factor formation contractile clearly demonstrates continuous factor/NO occurs isolated vascular whole animals.