Xie Y, Garban H, Ng C, Rajfer J, Gonzalez-Cadavid N F
Department of Surgery, UCLA School of Medicine, Harbor-UCLA Medical Center, Torrance 90509, USA.
J Urol. 1997 Mar;157(3):1121-6.
Given that smoking is a risk factor for erectile dysfunction, this study aimed to determine, in a rat model, whether long-term exposure to cigarette smoke impairs nitric oxide (NO)-dependent erectile function and reduces penile nitric oxide synthase (NOS), and if these changes are accompanied with effects on the systemic blood pressure.
Adult (5 month) and old (20 month) rats were exposed to daily passive smoking for 8 wks. Three days after the conclusion of exposure, half of the animals were submitted to electrical field stimulation (EFS) of the cavernosal nerve and the maximum intracavernosal pressure (MIP) and mean arterial pressure (MAP) were determined and expressed as mm. Hg. On the other half of the animals, NOS activity in the penile cytosol was measured by the arginine/citrulline assay, and neuronal NOS (nNOS) and endothelial NOS (eNOS) contents were estimated by western blot and densitometry.
When compared to controls, the smoking rats had a higher MAP in both the adult (115 vs 162) and old (113 vs 140) rats, but surprisingly the MIP also increased, from 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 affected. Nitrite release, in vitro, by cavernosa slices or in rat penile smooth muscle cells (RPSMC) was not inhibited by nicotine or cotinine.
These results indicate that chronic smoking in the rat leads 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.
鉴于吸烟是勃起功能障碍的一个危险因素，本研究旨在通过大鼠模型确定长期暴露于香烟烟雾是否会损害一氧化氮（NO）依赖的勃起功能并降低阴茎一氧化氮合酶（NOS），以及这些变化是否伴随着对全身血压的影响。
成年（5个月）和老年（20个月）大鼠每天接受被动吸烟，持续8周。暴露结束后三天，将一半动物进行海绵体神经的电场刺激（EFS），并测定最大海绵体内压（MIP）和平均动脉压（MAP），结果以毫米汞柱（mm. Hg）表示。对另一半动物，通过精氨酸/瓜氨酸测定法测量阴茎细胞溶质中的NOS活性，并通过蛋白质印迹法和光密度测定法估计神经元型NOS（nNOS）和内皮型NOS（eNOS）的含量。
与对照组相比，吸烟大鼠在成年（115对162）和老年（113对140）大鼠中均具有较高的MAP，但令人惊讶的是MIP也增加了，从78增加到111（成年大鼠），从59增加到83（老年大鼠）。吸烟使成年大鼠阴茎NOS活性降低73%，老年大鼠降低62%，nNOS含量分别降低43%和50%。相比之下，eNOS未受影响。海绵体切片或大鼠阴茎平滑肌细胞（RPSMC）在体外的亚硝酸盐释放不受尼古丁或可替宁的抑制。
这些结果表明，大鼠慢性吸烟会导致与年龄无关的中度高血压以及阴茎NOS活性和nNOS含量显著降低，这在对EFS的勃起反应降低中未得到体现，也未伴随着阴茎eNOS的减少。
