Objectives: To determine whether nitric oxide (NO) is a mediator of prostatic smooth muscle activity. Methods: Pharmacologic experiments using electrical field stimulation (EFS) were performed on strips of human and canine prostate. Results: EFS alone elicited frequency-dependent contractions in preparations of human and canine prostates. The greatest contractile activity was achieved at 30 Hz. In the presence of 10-5 M guanethidine (GUA) and 2 × 10-1 M atropine (ATR), EFS elicited relaxation of canine prostate strips relative to baseline tension. A weak biphasic response consisting of initial relaxation and subsequent contraction relative to baseline tension was observed in the human prostate strips exposed to similar conditions. The smooth muscle activity observed in the presence of GUA plus ATR was attributed to nonadrenergic, noncholinergic (NANC) nerve transmission. 10-4 M L-NG-nitroarginine methylester (NAME) significantly increased EFS-elicited NANC smooth muscle activity both in human and canine prostates. L-arginine, 10-2 M, reversed the effect of L-NAME in human and canine prostates. Sodium nitroprusside, 10-4 M, a donor of NO, caused relaxation of both human and canine prostates. The mean magnitude of the relaxant response/cross-sectional area in human prostate (2.64 ± 0.4 g/cm2) was significantly greater than in the canine prostate (1.09 ± 0.17 g/cm2) (P < 0.005). Conclusions: These results provide compelling evidence that NO plays a role in mediating contractile function of human and canine prostates.
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