¹Departments of Pharmacology and Toxicology, Kingston, Ontario, Canada

²Department of Urology, Queen's University, Kingston, Ontario, Canada

³The Human Sexuality Group, Kingston General Hospital, Kingston, Ontario, Canada

Correspondence to: M A Adams, Department of Pharmacology and Toxicology, Queen's University, Kingston, Ontario, Canada, K7L 3N6. E-mail: adams@post.queensu.ca

As part of the multifactorial nature of erectile dysfunction, anxiety associated with sexual performance (SPA) remains a major contributing factor to its progression. In fact, the heightened sympathetic activity associated with sexual performance anxiety may be a key early component of this disruption of normal erectile responses. We are not aware that any animal models have been developed to assess this phenomenon. Using apomorphine (APO, 80 g/kg s.c.)-induced erections in rats we characterised the effects of behavioural or pharmacological hyperadrenergic stimulation (that is, anxiety) on erections and hemodynamics. We developed an experimental SPA paradigm by exposing male rats to the stress of being observed by a larger, older male rat placed in close proximity to test rats during APO testing. In a separate group, adrenergic stress was simulated using a sympathomimetic, methoxamine (MXA) given prior to APO testing. In a third group, the changes in circulatory parameters (mean arterial pressure, heart rate) were determined following instrumentation with radiotelemetric transducers for each scenario. APO-induced erections were significantly lower in both the behavioural (1.25±0.8) and pharmacological (0.33±0.5) stressor paradigms compared to controls (2.81±0.9). Further, erections in MXA-treated rats were significantly lower than in the observed scenario. Despite the differences in erections hemodynamic assessments showed no differences in MAP or HR changes between the different experimental conditions. Thus, both the behavioural and pharmacological paradigms of SPA decreased erections, but did not affect the circulation. This suggests that the level of hyperadrenergic input required to induce erectile dysfunction can be subtle, and target only erectogenic pathways.

International Journal of Impotence Research (2002) 14, 107-115. DOI:10.1038/sj/ijir/3900836

erectile dysfunction; apomorphine; anxiety