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<scp>l</scp>-Arginine–Induced Conducted Signals Alter Upstream Arteriolar Responsivity to<scp>l</scp>-Arginine

46

Citations

39

References

1995

Year

Abstract

Abstract 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 to 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.

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