抄録
Inhibitory neurotransmission in guinea pig lower esophageal sphincter (LES) muscles was investigated by using electrophysiological methods. Transmural nerve stimulation (TNS) initiated an inhibitory junction potential (i.j.p.); the amplitude increased 35% by atropine (10-6 M) and converted to a muscarinic excitatory junction potential (e.j.p.) by apamin (10-7 M) plus Nω-nitro-L-arginine (L-NNA, 10-5 M). In atropinized tissue, the i.j.p. amplitude was reduced 58% by guanethidine (5×10-6 M), 41% by L-NNA (10-5 M), 57% by suramin (10-4 M), and it was abolished by apamin (10-7 M), suggesting that this potential was produced by ATP and nitric oxide (NO) released from adrenergic and nitrergic nerves, respectively, through the activation of Ca2+ -sensitive K+ channels. Hyperpolarizations produced by ATP and NO were inhibited by apamin. The i.j.p. amplitude was reduced after desensitizing the membrane with ATP. In atropinized tissue, TNS produced a relaxation that was reduced 15% by guanethidine (5×10-6 M), 50% by L-NNA (10-5 M), and 30% by apamin (10-7 M). Thus the LES receives cholinergic excitatory and adrenergic and nitrergic inhibitory innervations; the latter two components contribute evenly to the i.j.p. generation. The relaxation is mainly produced by NO in a membrane potential-independent way.
