Apamin-sensitive and -insensitive components of inhibitory junction potentials in rat caecum: role of nitric oxide.

1. The non-adrenergic non-cholinergic (NANC) inhibitory response to electrical field stimulation (EFS) in circular muscle from rat caecum was investigated using the single sucrose-gap technique. EFS with single pulses evoked hyperpolarization oral inhibitory function potential (IJP) of the membrane associated with muscular relaxation or with transient inhibition of spontaneous contractile activity. 2. The amplitude and the duration of the IJPs were enhanced by using train stimulation at increasing frequency. 3. Apamin (10(-7) M) reduced the amplitude of IJPs at all frequencies tested. 4. N omega-nitro-L-arginine methyl ester (L-NAME) (10(-4) M, 5 x 10(-4) M), but not D-NAME, caused a concentration dependent decrease in the amplitude of IJPs at all frequencies tested. L-Arginine (10(-3) M) prevented these effects. 5. L-NAME (5 x 10(-4) M) caused the disappearance of the apamin-resistant IJP-component, evoked by single pulse or by low frequency trains. 6. Sodium nitroprusside (SNP) (10(-4) M), a nitric oxide (NO) donor, induced hyperpolarization of membrane potential and muscular relaxation. SNP-induced effects were not affected by pretreatment of the muscle strips with effective concentrations of tetrodotoxin, apamin, and L-NAME. 7. P2-purinergic antagonists, reactive blue 2 (up to 5 x 10(-4) M) and suramin (up to 3 x 10(-4) M), failed to affect the evoked IJPs. 8. These results show that, in rat caecum, the NANC response to electrical stimulation is composed of two distinguishable components: an apamin-resistant and an apamin-sensitive component. NO or a related compound is mainly involved in the mediation of the apamin-resistant component, while ATP is not the mediator responsible for the apamin-sensitive component.