Aim
To investigate changes in the endothelial glycocalyx in the penile corpus cavernosum of the rat with low androgen status and its relationship with erection function.
Background
The endothelial glycocalyx is an important barrier that protects the structure and function of endothelial cells. Androgen deficiency is a common factor that causes structural and functional impairment of endothelial cells.
Conclusion
Low androgen status may suppress the level of nitric oxide in the cavernous tissue of the penis via impairment of the endothelial glycocalyx, resulting in inhibited erection function in rats.
Methods
Eighteen 10-week-old Sprague-Dawley male rats were randomly divided into 3 groups (n = 6 each): sham operation, castration, and castration + testosterone replacement. The maximum intracavernosal pressure/mean arterial pressure of the penis was measured after modeling for 4 weeks. The expression levels of endothelial nitric oxide synthase (eNOS), phospho-eNOS, syndecan 1, heparanase, and nitric oxide in penile cavernous tissue and the serum levels of heparan sulfate, hyaluronic acid, tumor necrosis factor α, and interleukin 6 were determined. Transmission electron microscopy was used to observe the ultrastructure of the endothelial glycocalyx in penile tissue. Outcomes: The thickness of the endothelial glycocalyx in the penile corpus cavernosum of castrated rats was significantly lower than that of the control group.
Results
In the castrated rats, the endothelial glycocalyx thickness, syndecan 1 level, ratio of phospho-eNOS to eNOS, nitric oxide level, and maximum intracavernosal pressure/mean arterial pressure (3 V, 5 V) were significantly lower than those in the sham group (P < .05). The expression of heparanase and the serum levels of tumor necrosis factor α and interleukin 6 were significantly higher in the castrated group than in the sham group (P < .05). Clinical translation: Upregulating the expression of the endothelial glycocalyx in the penile corpus cavernosum may be a new method for treating erectile dysfunction caused by low androgen levels. Strengths and limitations: This study confirms that low androgen status promotes the breakdown of the endothelial glycocalyx. However, further research is needed to determine whether androgens are related to the synthesis of the endothelial glycocalyx.