ArticleTranslational andrology and urology2026
Hypertension impairs erectile function in spontaneously hypertensive rats by suppressing adiponectin in the penile corpus cavernosum.
Article in Translational andrology and urology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Hypertension is a well-established risk factor for erectile dysfunction and is closely associated with endothelial dysfunction and reduced nitric oxide bioavailability; however, the underlying molecular mechanisms remain incompletely understood. This study aimed to investigate whether hypertension impairs erectile function by regulating adiponectin (APN) expression and the phosphoinositide 3-kinase/protein kinase B/endothelial nitric oxide synthase (PI3K/AKT/eNOS) signaling pathway in the penile corpus cavernosum and to explore whether APN-related PI3K/AKT/eNOS signaling may be involved in the beneficial effects of icariin (ICA) in spontaneously hypertensive rats (SHRs). Methods: Twelve-week-old Wistar-Kyoto (WKY) rats and SHRs were randomly assigned to six groups (n=6 per group) as follows: WKY, WKY + ICA, SHR, SHR + ICA, SHR + negative control (SHR + NC), and SHR + adeno-associated virus (SHR + AAV). Rats in the SHR + AAV group received an intracavernosal injection of an AAV vector carrying the Results: The NO levels in the penile corpus cavernosum and the ICPmax/MAP ratio were significantly lower in SHRs than in WKY rats. APN expression was markedly reduced in endothelial cells of the penile corpus cavernosum in SHRs, and the p-PI3K/PI3K, p-AKT/AKT, and p-eNOS/eNOS ratios in the penile corpus cavernosum were also significantly lower in SHRs than in WKY rats. Compared with the SHR group, both ICA treatment (SHR + ICA) and AAV-mediated APN overexpression (SHR + AAV) significantly increased NO production and the ICPmax/MAP ratio (P<0.05), accompanied by increased APN expression and enhanced phosphorylation of PI3K, AKT, and eNOS in the penile corpus cavernosum (P<0.05). Conclusions: Hypertension induces erectile dysfunction (ED) partly by downregulating APN expression in endothelial cells of the penile corpus cavernosum and suppressing the PI3K/AKT/eNOS signaling pathway. AAV-mediated APN overexpression upregulated APN expression, activated the PI3K/AKT/eNOS pathway, and improved erectile function in SHRs, whereas ICA treatment improved erectile function and may increase APN expression and enhance PI3K/AKT/eNOS signaling.
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