Extracellular arginine rapidly dilates in vivo intestinal arteries and arterioles through a nitric oxide mechanism

Objective: Arginine used for nitric oxide formation can be from intracellular stores or transported into cells. The study evaluated the rapidity, and primary site of NO and vascular resistance responses to arginine at near physiological concentrations (100–400 μ M). Methods: Arginine was applied to a single arteriole through a micropipette to determine the fastest possible responses. For vascular blood flow and [NO] responses, arginine was added to the bathing media. Results: Dilation of single arterioles to arginine began in 10–15 seconds and application over the entire vasculature increased [NO] in ～ 60–90 seconds, and flow increased within 120–300 seconds. Resting periarteriolar [NO] for arterioles was 493.6 ± 30.5 nM and increased to 696.1 ± 68.2 and 820.1 ± 110.5 nM at 200 and 400 μ M L‐arginine. The blood flow increased 50% at 400–1200 μ M L‐arginine. The reduced arterial resistance during topical arginine was significantly greater than microvascular resistance at 100 and 200 μ M arginine. All responses were blocked by L‐NAME. Conclusions: This study demonstrated arterial resistance responses are as or more responsive to arginine induced NO formation as arterioles at near physiological concentrations of arginine. The vascular NO and resistance responses occurred rapidly at L‐arginine concentrations at and below 400 μ M, which predict arginine transport processes were involved.