EFFECT OF LONG-TERM PASSIVE SMOKING ON ERECTILE FUNCTION AND PENILE NITRIC-OXIDE SYNTHASE IN THE RAT

Purpose: Given that smoking is a risk factor for erectile dysfunction, this study aimed to determine, in a rat model, whether long-term expo sure to cigarette smoke impairs nitric oxide (NO)-dependent erectile f unction and reduces penile nitric oxide synthase (NOS), and if these c hanges are accompanied with effects on the systemic blood pressure. Ma terials and Methods: Adult (5 month) and old (20 month) rats were expo sed to daily passive smoking for 8 wks. Three days after the conclusio n of exposure, half of the animals were submitted to electrical field stimulation (EFS) of the cavernosal nerve and the maximum intracaverno sal pressure (MIP) and mean arterial pressure (MAP) were determined an d expressed as mm. Hg. On the other half of the animals, NOS activity in the penile cytosol was measured by the arginine/citrulline assay, a nd neuronal NOS (nNOS) and endothelial NOS (eNOS) contents were estima ted by western blot and densitometry. Results: When compared to contro ls, the smoking rats had a higher MAP in both the adult (115 vs 162) a nd old (113 vs 140) rats, but surprisingly the MIP also increased, fro m 78 to 111 (adult rats) and from 59 to 83 (old rats). Smoking reduced penile NOS activity by 73% (adult rats), and 62% (old rats), and nNOS content by 43% and 50%, respectively. In contrast, eNOS was not affec ted. Nitrite release, in vitro, by cavernosa slices or in rat penile s mooth muscle cells (RPSMC) was not inhibited by nicotine or cotinine. Conclusion: These results indicate that chronic smoking in the rat lea ds to age-independent moderate hypertension and considerable decreases in penile NOS activity and nNOS content, that are not reflected in a reduction of the erectile response to EFS or accompanied by a decrease in penile eNOS.