Distinct mechanisms implicated in atherosclerosis-induced erectile dysfunction in rabbits

Ageing and atherosclerosis (ATH) are well-known risk factors for erectile dysfunction (ED). To identify the mechanisms implicated in ATH-induced ED. independently of its ageing-associated component, we studied (i) erectile responses in vivo. and, 60 endothelium-dependent and independent relaxations of corporal strips from young adult (YAD, n = 6), adult (AD. 11 = 6). and cholesterol-fed (ATH, n = 8) New-Zealand white rabbits. Measurement of Intima Media (1, M) ratio on iliac arteries from ATH rabbits determined those with moderate (Mod ATH. 0.5 +/- 0.3) or severe (Sev ATH, 1.5 +/-0.4, P < 0.05 Mann-Whitney) atherosclerotic lesions. Erectile response,,, were reduced in AD compared with YAD rabbits (at 6 V to 10 Hz: 51.6+/-4.6%,, vs. 57.5 +/- 1.4%) them ere similar in AD and mod ATH rabbits (48.1 +/- 4.6%) but drastically impaired in Se ATH rabbits (34.8 +/- 5.4%, P < 0.05. two-way analysis of variance (ANOVA)). Corporal endothelium-dependent and -independent relaxations were comparable in YAD and AD rabbits (maximal relaxation to acetylcholine: 51.3 +/- 9.5 vs. 56.1 +/- 9.3%) but decreased in ATH est that the mechanisms implicated in ATH-induced ED are rabbits (37.1 +/- 1.6%, P <0.001, two-way ANOVA). These results suggest that the mechanisms implicated in ATH-induced ED are distinct from the ageing-related process in rabbits. Thus, future therapeutic targets to treat or present ATH-induced ED may include the reduction of the atherosclerotic plaque size or progression, as well as an improvement of the smooth muscle and endothelial reactivity of the corpus cavernosum. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.