HHS Public Access Author manuscript Author Manuscript
Andrology. Author manuscript; available in PMC 2017 September 01. Published in final edited form as: Andrology. 2016 September ; 4(5): 977–983. doi:10.1111/andr.12218.
Mechanistic link between erectile dysfunction and systemic endothelial dysfunction in type 2 diabetic rats Biljana Musicki1, Johanna L. Hannan2, Gwen Lagoda1, Trinity J. Bivalacqua1, and Arthur L. Burnett1 1The
James Buchanan Brady Urological Institute and Department of Urology, The Johns Hopkins School of Medicine, Baltimore, Maryland, USA
Author Manuscript
2Department
of Physiology, Brody School of Medicine, East Carolina University, Greenville, North Carolina, USA
Abstract
Author Manuscript Author Manuscript
Men with type 2 diabetes mellitus (T2DM) and erectile dysfunction (ED) have greater risk of cardiovascular events than T2DM men without ED, suggesting ED as a predictor of cardiovascular events in diabetic men. However, molecular mechanisms underlying endothelial dysfunction in the diabetic penis explaining these clinical observations are not known. We evaluated whether the temporal relationship between ED and endothelial dysfunction in the systemic vasculature in T2DM involves earlier redox imbalance and endothelial nitric oxidase synthase (eNOS) dysfunction in the penis than in the systemic vasculature, such as the carotid artery. Rats were rendered T2DM by high-fat diet for 2 weeks, followed by an injection with low-dose streptozotocin. After 3 weeks, erectile function (intracavernosal pressure) was measured and penes and carotid arteries were collected for molecular analyses of eNOS uncoupling, protein Sglutathionylation, oxidative stress (4-hydroxy-2-nonenal, 4-HNE), protein expression of NADPH oxidase subunit gp91phox, endothelium-dependent vasodilation in the carotid artery, and nonandrenergic, non-cholinergic (NANC) mediated cavernosal relaxation. Erectile response to electrical stimulation of the cavernous nerve and NANC mediated cavernosal relaxation were decreased (p
Andrology. Author manuscript; available in PMC 2017 September 01. Published in final edited form as: Andrology. 2016 September ; 4(5): 977–983. doi:10.1111/andr.12218.
Mechanistic link between erectile dysfunction and systemic endothelial dysfunction in type 2 diabetic rats Biljana Musicki1, Johanna L. Hannan2, Gwen Lagoda1, Trinity J. Bivalacqua1, and Arthur L. Burnett1 1The
James Buchanan Brady Urological Institute and Department of Urology, The Johns Hopkins School of Medicine, Baltimore, Maryland, USA
Author Manuscript
2Department
of Physiology, Brody School of Medicine, East Carolina University, Greenville, North Carolina, USA
Abstract
Author Manuscript Author Manuscript
Men with type 2 diabetes mellitus (T2DM) and erectile dysfunction (ED) have greater risk of cardiovascular events than T2DM men without ED, suggesting ED as a predictor of cardiovascular events in diabetic men. However, molecular mechanisms underlying endothelial dysfunction in the diabetic penis explaining these clinical observations are not known. We evaluated whether the temporal relationship between ED and endothelial dysfunction in the systemic vasculature in T2DM involves earlier redox imbalance and endothelial nitric oxidase synthase (eNOS) dysfunction in the penis than in the systemic vasculature, such as the carotid artery. Rats were rendered T2DM by high-fat diet for 2 weeks, followed by an injection with low-dose streptozotocin. After 3 weeks, erectile function (intracavernosal pressure) was measured and penes and carotid arteries were collected for molecular analyses of eNOS uncoupling, protein Sglutathionylation, oxidative stress (4-hydroxy-2-nonenal, 4-HNE), protein expression of NADPH oxidase subunit gp91phox, endothelium-dependent vasodilation in the carotid artery, and nonandrenergic, non-cholinergic (NANC) mediated cavernosal relaxation. Erectile response to electrical stimulation of the cavernous nerve and NANC mediated cavernosal relaxation were decreased (p
