As S-nitrosothiols were proposed as nitrergic carriers in vascular and nonvascular smooth muscle, we have investigated the relaxant properties of several S-nitrosothiols in the porcine retractor penis(PRP) muscle and compared them with the effects of exogenously added NO, electrical field stimulation(EFS) of NANC nerves and sodium nitroprusside(SNP). Also the influences of oxyhemoglobin and hydroquinone on the relaxant responses were investigated. In addition, effects of NO on membrane potentials and its involvement in the generation of inhibitory junction potential(IJP) were investigated with conventional intracellular microelectrode technique. The results were summerized as follows.
1. Frequency-dependent relaxations of PRP muscle were induced by EFS to NANC nerve. Tetrodotoxin(1×l0^(-6)M) abolished the relaxations of PRP muscle induced by EFS, and L-NAME((2×10^(-5)M) and methylene blue(4×10^(-5)M) inhibited the relaxations. L-NAME-induced inhibition of the relaxations was reversed by L-arginine(1×10^-3M), but not by D-arginine.
2. Exogenous NO(1×10^(-5)-1×10^(-4)M), sodium nitroprusside((1×10^(-7)-1×10^(-4)M) induced dose-dependent relaxations of PRP muscle. All S-nitrosothiols(1×10^(-7)-1×10^(-4)M) tested relaxed the PRP muscle in dose-dependent manner and the potency order was SNAP> GSNO> CysNO> SNAC
3. Oxyhemoglobin(5×10^(-5)M) blocked the relaxation induced by exogenous NO and inhibited EFS-, S-nitrosothiols-, and SNP-induced relaxation.
4. Hydroquinone(1×10^(-4)M) also abolished the relaxations induced by exogenous NO, and reduced the relaxations induced by S-nitrosothiols, but did not affect EFS- and SNP-induced relaxations.
5. SNP(2×10^(-6)-5×10^(-6)M) relaxed muscle strips but the membrane potentials were not affected.
6. EFS with several pulses(1㎳, 2㎐, 80V) produced an inhibitory junction potential(IJP) with muscle relaxation. They were abolished by TTX(2X10^(-6)M). N^G-nitro-L-arginine(L-NNA, 2×10^(-5)M) abolished the muscle relaxation, but had no effect on IJP.
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