Related Experiment Video
Updated: Jul 16, 2026
Intracavernosal Pressure Recording to Evaluate Erectile Function in Rodents
Published on: June 6, 2018
Altered penile vascular reactivity and erection in the Zucker obese-diabetic rat
Christopher Wingard1, David Fulton, Shahid Husain
1Brody School of Medicine at East Carolina University-Physiology, Greenville, NC, USA. wingarddc.ecu.edu
Introduction:
The combination of the independent risk factors for erectile dysfunction, obesity, hypertension, and diabetes are manifested collectively in a condition known as metabolic syndrome X. However, the exact mechanism(s) by which the combination of these factors contributes to erectile dysfunction have yet to be elucidated.
Aim:
We hypothesized that protein kinase C (PKC) and Rho-kinase enhanced vascular tone and thus contributed to erectile dysfunction in this condition.
Methods:
Erectile function was evaluated by recording voltage-dependent increases in intracavernosal pressure following stimulation of the cavernosal nerve in 16- to 20-week-old lean and obese-diabetic Zucker rats. Cavernosal tissue contractile and relaxation responses were evaluated in vitro when contracted with phenylephrine, endothelin-1 and relaxed by Rho-kinase, PKC inhibitors or sodium nitroprusside. Additionally, cavernosal tissue Rho-kinase, protein kinase, and nitric oxide synthase isoform expression were evaluated by Western blot.
Results:
The voltage-dependent erectile responses were suppressed by >30% in the obese-diabetic Zucker rat. The maximal stress generated by cavernosal tissue from the obese-diabetic was significantly greater than the lean response by greater than 0.8 mN/mm(2) for both phenylephrine and endothelin stimulation. The PKC inhibitor, chelerythrine, inhibited more than 30% of the phenylephrine-induced and 70% of the endothelin-1-induced contractions. Rho-kinase inhibition, with either Y-27632 or HA-1077, revealed impaired relaxations of nearly 30% in tissue from obese-diabetic animals. Western blot analysis revealed increased protein expression of PKC alpha and delta and Rho-kinase alpha and beta but no loss for endothelial or neuronal nitric oxide synthase.
Conclusions:
In this rodent model both PKC and Rho-kinase signaling elements may contribute to an enhanced vasoconstriction state of the penile smooth muscle that was differentially dependent on the agonist used. The enhanced vasoconstrictive state of the tissue could contribute to the reduced voltage-dependent erectile response in the obese-diabetic Zucker rat.
Insights
Metabolic syndrome contributes to erectile dysfunction by enhancing vasoconstriction in penile smooth muscle. Protein kinase C (PKC) and Rho-kinase signaling are implicated in this enhanced vascular tone, leading to reduced erectile function.
Area of Science:
- Physiology
- Endocrinology
- Urology
Background:
- Metabolic syndrome, characterized by obesity, hypertension, and diabetes, is linked to erectile dysfunction.
- The precise mechanisms by which metabolic syndrome impairs erectile function remain unclear.
Purpose of the Study:
- To investigate the roles of protein kinase C (PKC) and Rho-kinase in enhanced vascular tone contributing to erectile dysfunction in obese-diabetic rats.
- To elucidate the signaling pathways involved in metabolic syndrome-associated erectile dysfunction.
Main Methods:
- Erectile function was assessed in Zucker rats via intracavernosal pressure measurements.
- In vitro studies evaluated penile tissue contractility and relaxation responses to various stimuli and inhibitors.
- Western blot analysis quantified protein expression of key signaling molecules.
Main Results:
- Obese-diabetic rats exhibited significantly suppressed erectile responses.
- Penile tissues showed increased contractility and impaired relaxation in response to PKC and Rho-kinase inhibition.
- Elevated expression of PKC and Rho-kinase proteins was observed, with no change in nitric oxide synthase isoforms.
Conclusions:
- PKC and Rho-kinase signaling contribute to enhanced vasoconstriction in penile smooth muscle of obese-diabetic rats.
- This enhanced vasoconstriction is a potential mechanism underlying reduced erectile function in metabolic syndrome.