Vascular Myocyte-Derived Nitric Oxide Is an Autocrine That Limits Vasoconstriction

Abstract

Vascular myocytes and endothelial cells possess the enzymatic machinery to generate nitric oxide from L-arginine. This study tests the hypothesis that myocyte-derived nitric oxide has an autocrine function to inhibit contraction. Rat aortic rings were placed in muscle baths for isometric force measurement. Denuded and intact rings contracted to N[omega]nitro-L-arginine; L-arginine reversed these contractions. Compared to intact rings, contractile sensitivity to phenylephrine was increased in denuded rings; N[omega]nitro-L-arginine caused a further enhancement of phenylephrine sensitivity. Acetylcholine contracted denuded rings but not intact rings; these contractions were also potentiated by N[omega]nitro-L-arginine. In intact rings contracted with phenylephrine, acetylcholine caused relaxation that was inhibited by N[omega]nitro-L-arginine. Denuded rings did not relax to acetylcholine. In summary, contractile responses of rat aortae to interventions that alter nitric oxide production are the composite of enzymatic activity in both the endothelial cells and myocytes. Thus, myocyte-derived nitric oxide modulates vascular tone.