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Vol. 283, Issue 2, 684-691, 1997
Department of Transplant Surgery, Medical College of Wisconsin,
Milwaukee Wisconsin
Arginine is a precursor amino acid for the synthesis of nitric oxide by
nitric oxide synthase. A defect in arginine supply could regulate
nitric oxide-mediated, endothelium-dependent relaxation. In this study,
we evaluated the effect of supplementation with L-arginine
given in vitro on both functional relaxation and cGMP generation in response to acetylcholine in the streptozotocin-induced diabetic rat aorta. The concentration of arginine in plasma and aortic
tissue were both decreased by diabetes. Acute incubation in
vitro with L-arginine augmented the impaired
relaxation to acetylcholine in diabetic rings although not altering
relaxation in control rings. L-Arginine also enhanced
relaxation to acetylcholine in diabetic rings incubated in the presence
of either indomethacin or tetraethylammonium to inhibit cyclooxygenase
activity and potassium channel activity, respectively.
Acetylcholine-stimulated cGMP generation (which was blocked by
L-nitroarginine) was diminished in diabetic rings compared
with control rings. L-Arginine restored cGMP in diabetic
rings (with but not without endothelium) to levels similar to control
rings. L-Arginine did not alter cGMP generated by
nitroglycerin. Incubation with L-arginine had no effect on acetylcholine-stimulated cGMP generation in control rings (with and
without endothelium). These data suggest a potential intracellular substrate deficiency in nitric oxide production by diabetic endothelium which can be overcome acutely in vitro by provision of
substrate for nitric oxide synthase.
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