Many physiologic studies have been carried out to identify the neurotransmitters involved in regulating the motility of the smooth muscle in the vas deferens, but the transmitter of a non-adrenergic and non-cholinergic inhibitory nerves has not
been
clearly identified. We investigated the role of nitric oxide in response to sympathetic motor activity in the rat vas deferens.
1. Nitroprusside and L-NAME had neither contractile nor relaxing effects directly.
On the stabilized muscle strips of rat vas deferens, norepinephrine induced a phasic contraction for 10 seconds followed by the sustained tonic contraction. The phasic contraction of norepinephrine was increased by the pretreatment of
nitroprusside(P>0.05) and decreased by L-NAME(p<0.01). This tonic contraction was decreased dose-dependently by the pretreatment of nitroprusside(p<0.01), and increased by L-NAME(P<0.01).
On the muscle strips of rat vas deferens, submaximally precontracted with norepinephrine, nitroprusside potentiated the contraction, followed by the delayed, sustained relaxation, which was blocked by L-NAME.
2. On the muscle strips of rat vas deferens, electrical field stimulation induced an initial phasic contraction for 2-3 seconds, followed by the tonic contraction, which was blocked by L-NAME dose-dependently.
The phasic contraction of electrical field stimulation was increased by the pretreatment of nitroprusside(P>0.05) and decreased by L-NAME(p<0.01). This tonic contraction was decreased by the pretreatment of nitroprusside dose-dependently(P<0.01),
and
increased by L-NAME(P<0.01).
With these results, nitric oxide has the excitatory effect at the phasic contraction, and the inhibitory effect at the tonic contraction in response to sympathetic motor activity in the rat vas deferens partially.
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