Evidence that both nitric oxide (NO) and a non‐NO hyperpolarizing factor elicit NANC nerve‐mediated relaxation in the rat isolated anococcygeus

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Abstract
Responses to electrical field stimulation (EFS; 0.5–10 Hz, 0.2 ms duration, supramaximal voltage for 20 s) of non‐adrenergic, non‐cholinergic, (NANC) nerves were obtained in preparations of rat anococcygeus pre‐contracted with titrated concentrations of phenylephrine (0.1–1 μM) to ∼40% of their maximum contraction to phenylephrine (Fmax) regardless of drug treatment. With this set level of active force, NANC nerve stimulation resulted in relaxations that were maximal (peak relaxation) at 0.5–1 Hz, abolished by tetrodotoxin (1 μM) but only minimally blocked by the nitric oxide synthase (NOS) inhibitor, NG‐nitro‐L‐arginine, (L‐NOARG; 100 μM). Furthermore, the nitric oxide (NO) scavenger, oxyhaemoglobin (HbO; 30 μM) gave no further block alone or in combination with L‐NOARG (100 μM). By comparison, in preparations contracted with phenylephrine to ∼70% Fmax, relaxations to NANC nerve stimulation were markedly reduced or abolished by combined treatment with L‐NOARG (100 μM) and HbO (30 μM). Nifedipine (0.3 μM) significantly inhibited NANC nerve‐mediated relaxations, which became frequency‐dependent and abolished those resistant to L‐NOARG (100 μM) and HbO (30 μM). These data suggest that a non‐NO, hyperpolarizing factor and NO both contribute to NANC nerve‐mediated inhibitory responses in the rat anococcygeus. However, responses to the non‐NO factor were observed only in preparations contracted sub‐maximally by a nifedipine‐sensitive mechanism.

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