Properties of the inhibitory junction potential in smooth muscle of the guinea-pig gastric fundus

1 In circular smooth muscle of the guinea-pig gastric fundus, transmural nerve stimulation evoked a cholinergic excitatory junction potential (e.j.p.), and blockade of the e.j.p. by atropine revealed a nonadrenergic non-cholinergic (NANC) inhibitory junction potential (i.j.p.). 2 The amplitude of the e.j.p. was increased by apamin, suramin or N(G)nitro-L-arginine (L-NOARG), with no significant change in the membrane potential. 3 The i.j.p. consisted of two components (fast and slow); apamin inhibited the former, nitroarginine inhibited the latter, and suramin inhibited both components. 4 Apamin inhibited the hyperpolarization produced by adenosine 5'-triphosphate (ATP) but not by vasoactive intestinal polypeptide (VIP). Suramin inhibited the hyperpolarization produced by VIP but not by ATP. The sodium nitroprusside (SNP)-induced hyperpolarization was not blocked by apamin or suramin. L-NOARG or tetrodotoxin did not inhibit the hyperpolarization produced by ATP, VIP or SNP. 5 The data did not support the hypothesis that ATP, VIP or nitric oxide (NO) is the main transmitter responsible for generation of the NANC i.j.p. in the fundus. 6 Actions of L-NOARG suggest that endogenous NO may be involved in junctional transmission, mainly as an inhibitory modulator of cholinergic transmission.