Abstract
IntroductionDisturbances in thyroid function lead to sexual dysfunction in humans. However, the mechanisms by which hyperthyroidism causes erectile dysfunction (ED) are unknown. Whereas nitric oxide (NO) is the mediator of erection, sympathetic activation causes detumescence.ObjectiveWe hypothesized that hyperthyroidism increases sympathetic‐mediated contractility in cavernosal tissue.Methods and ResultsWistar male rats were submitted to experimental hyperthyroidism (70ug/Kg T3 for 14 days). Thyroid hormone T3 plasmatic levels were increased in hyperthyroid animals (Hyper) (Control: 0.43±0.08 vs Hyper: 1.45±0.64, ng/mL). After euthanasia, penises were excised and dissected. Cavernosal strips were mounted in a myograph and stretched to a resting force of 3.0 mN. Cavernosal contractility to phenylephrine (PE) (Control: 1.72±0.2 vs Hyper: 3.06±0.2, mN) and sympathetic‐nerve stimulation (Control: 0.9±0.4 vs Hyper: 2.03±0.3, mN) were increased in Hyper rats. Cavernosal responses to nonadrenergic‐noncholinergic‐mediated relaxation and endothelium‐independent relaxation were not altered.ConclusionOur results suggest that increased sympathetic‐ mediated responses contribute to ED in hyperthyroidism.
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