Nitric oxide release in penile corpora cavernosa in a rat model of erection

1. Nitric oxide (NO) levels were measured in the corpus cavernosum of ureth ane-anaesthetized rats by using differential normal pulse voltammetry with carbon fibre microelectrodes coated with a polymeric porphyrin and a cation exchanger (Nafion). A NO oxidation peak could be recorded at 650 mV vs. a Ag-AgCl reference electrode every 100 s. 2. This NO signal was greatly decreased by the NO synthase inhibitor N-G-ni tro-L-arginine methyl ester (L-NAME), given by local and systemic routes, a nd enhanced by the NO precursor L-arginine. Treatment with L-arginine rever sed the effect of L-NAME on the NO peak. 3. Both the NO signal and the intracavernosal pressure (ICP) were increased by electrical stimulation of cavernosal nerves (ESCN). However, the rise i n the NO levels long outlived the rapid return to baseline of the ICP value s at the end of nerve stimulation. 4. The ICP and the NO responses to ESCN were suppressed by local and system ic injections of L-NAME. Subsequent treatment with L-arginine of L-NAME-tre ated animals restored the NO signal to basal levels and the NO response to ESCN. The ICP response to ESCN was restored only in part by L-arginine. 5. The observed temporal dissociation between the NO and ICP responses coul d be accounted for by several factors, including the buffering of NO by the blood filling the cavernosal spaces during erection. 6. These findings indicate that an increased production of NO in the corpor a cavernosa is necessary but not sufficient for maintaining penile erection and suggest a complex modulation of the NO-cGMP-cavernosal smooth muscle r elaxation cascade.