Introduction. Elastin fibers confer passive recoil to many tissues including the lung, skin, and arteries. In the penis, elastin is present in sinusoids, arterioles, and in the tunica albuginea. Although decreased penile elastin has been reported in men with erectile dysfunction, the exact role of elastin in physiologic processes integral to erection remains speculative. Aim. The aim of this study was to characterize erectile function in elastin-deficient mice. Methods. Elastin haploinsufficient mice (Eln+/-) and aged match Eln+/+ (Wt) mice were used. Cavernosum was removed from some mice for quantification of elastin, collagen, and smooth muscle actin. Ex vivo assessment of contractile force generation was performed by myography. In vivo assessment of intracorporal pressure normalized to mean arterial pressure in response to electrical stimulation of the cavernosal nerve was measured. Veno-occlusive function was determined by cavernosography. Main Outcome Measures. The main outcome measures of this study were the in vitro and in vivo assessment of cavernosal vasoreactivity, veno-occlusive function and erection in mice deficient in elastin. Results. Eln +/- mice exhibited ~33% less penile elastin than Wt mice, with no change in collagen. Cavernosal tissue from Eln+/- mice has a significantly heightened contractile response, explained in part by increased smooth muscle cell content. Veno-occlusive function was significantly altered in Eln+/- mice. Interestingly, erectile function was impaired only at submaximal voltage (1V) stimulation (there was no impairment during the higher 2-V stimulus). Conclusions. Eln +/- mice display a cavernosal phenotype consistent with developmental changes attributable to the loss of elastin. These alterations confer a degree of altered erectile function that is able to be overridden by maximal stimulatory input. Altogether, these data suggest that elastin is important for erectile function.
- Animal models
- Sexual dysfunction introduction