Endothelium‐dependent modulation of resistance vessel contraction: studies with NG‐nitro‐l‐arginine methyl ester and NG‐nitro‐l‐arginine

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Abstract
The effect of NG‐nitro‐l‐arginine methyl ester (l‐NAME) and NG‐nitro‐l‐arginine (l‐NOARG) on noradrenaline (NA)‐induced contractility and acetylcholine (ACh)‐induced endothelium‐dependent relaxation was studied in rat mesenteric resistance arteries. Third order branches of mesenteric arteries were dissected and mounted on two forty micron wires in a Mulvany myograph. Incubation with l‐NAME and l‐NOARG (10 μm) caused a time‐dependent shift in the 50% response to NA (ED50) (0.01 μm‐10 μm) but was not associated with an increase in the maximum contractile response. l‐NAME and l‐NOARG (10 μm) caused a time‐dependent inhibition of ACh (1 μm)‐induced relaxation with a maximum effect after 120 min. Following endothelium removal, incubation with either l‐NAME or l‐NOARG caused no significant shift in the ED50, although the residual relaxation response to ACh (1 μm) was further attenuated.6 Incubation with the cylco‐oxygenase inhibitor, indomethacin, enhanced the relaxation to ACh and reduced the inhibitory effects of l‐NAME and l‐NOARG.7 In conclusion, l‐NAME and l‐NOARG are potent inhibitors of acetylcholine‐induced endothelium‐dependent relaxation in mesenteric resistance arteries. The shift in ED50 associated wtih these inhibitors suggests a probable role for the endothelium in modulating the contractility of the resistance vasculature.