L-arginine-induced conducted signals alter upstream arteriolar responsivity to L-arginine

Our purpose was to determine whether L-arginine was involved in vascular communication between downstream and upstream locations within a defined microvascular region. Arteriolar diameter was measured for the branches along a transverse arteriole in the superfused cremaster of anesthetized (pentobarbital sodium, 70 mg/kg IP) hamsters (N=53). The upstream branch arterioles dilated significantly to locally applied L-arginine (100 μmol/L pipette concentration) only if the downstream branches (≃1400 μm away) were preexposed. With exposure order downstream to upstream, diameter change was last branch, -3.8±1.5% (of baseline); third, +58.1±27%; first, +92±26% (n=5); with exposure order upstream to downstream: first branch, -0.4±3%; third, +5±11%; last, -5.6±7.5% (n=4). Thus, downstream preexposure applied L-arginine altered the responsivity upstream to locally applied L-arginine. Downstream-applied L-arginine also induced a conducted vasodilation (+17.8±2.8%; n=14) 1327±166 μm upstream. This response was completely blocked by simultaneous sucrose (600 mOsm), halothane (0.0345%), or N(ω)- nitro-L-arginine (L-NNA, 100 μmol/L) exposure to the feed vessel (second micropipette) midway between the downstream site of L-arginine exposure and the upstream observation site. An acetylcholine-induced conducted vasodilation (+18.1±2.6%, n=8) was also completely blocked by sucrose, halothane, or L-NNA. The change in responsivity upstream to locally applied L-arginine was not seen in the absence of a conducted vasodilation or when the conducted signal pathway was blocked after the conducted vasodilation was observed, and it could be triggered by a conducted response to acetylcholine as well as to L-arginine. Thus, the change in local responsivity upstream requires an ongoing conducted signal from downstream. Conducted signals likely play a dynamic role in the regulation of vascular responsivity within a defined microvascular region.