BACKGROUND: The relaxatory effect of acetylcholine was investigated on the feline internal anal sphincter (IAS), in vitro. RESULTS: Acetylcholine (10, 30, 100, and 1000 microM) caused a concentration-dependent relaxation of the same magnitude in strips from the proximal and distal IAS. The antagonist of nitric oxide synthase, N omega-nitro-L-arginine (L-NNA; 1, 10, and 100 microM), in a concentration-dependent and stereospecific manner, blocked the acetylcholine-induced relaxation, leaving a residual response of 10-30%. The blocking effect of L-NNA (100 microM) could not be shown in tissues that had been incubated with the substrate for nitric oxide synthase, L-arginine (1 mM). CONCLUSIONS: The present results suggest that the acetylcholine-induced relaxation of the IAS to a major extent is due to an activation of nitrergic, inhibitory motor neurons to the IAS.
BACKGROUND: The relaxatory effect of acetylcholine was investigated on the feline internal anal sphincter (IAS), in vitro. RESULTS:Acetylcholine (10, 30, 100, and 1000 microM) caused a concentration-dependent relaxation of the same magnitude in strips from the proximal and distal IAS. The antagonist of nitric oxide synthase, N omega-nitro-L-arginine (L-NNA; 1, 10, and 100 microM), in a concentration-dependent and stereospecific manner, blocked the acetylcholine-induced relaxation, leaving a residual response of 10-30%. The blocking effect of L-NNA (100 microM) could not be shown in tissues that had been incubated with the substrate for nitric oxide synthase, L-arginine (1 mM). CONCLUSIONS: The present results suggest that the acetylcholine-induced relaxation of the IAS to a major extent is due to an activation of nitrergic, inhibitory motor neurons to the IAS.