Journal
INTERNATIONAL JOURNAL OF IMPOTENCE RESEARCH
Volume 19, Issue 2, Pages 129-138Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/sj.ijir.3901494
Keywords
hyperglycemia; eNOS; NO; NO-independent endothelial relaxing factors; RhoA/Rho-kinase; oxidative stress
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Funding
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK067223, K08DK002568] Funding Source: NIH RePORTER
- NIDDK NIH HHS [DK 067223, DK 02568] Funding Source: Medline
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Erectile dysfunction (ED) is highly prevalent in diabetes mellitus. Pathophysiological mechanisms underlying diabetes-associated ED are in large part due to endothelial dysfunction, which functionally refers to the inability of the endothelium to produce vasorelaxing messengers and to maintain vasodilation and vascular homeostasis. The precise mechanisms leading to endothelial dysfunction in the diabetic vasculature, including the penis, are not yet fully understood. Hyperglycemia affects endothelial nitric oxide synthase activity and nitric oxide production/bioavailability, nitric oxide-independent relaxing factors, oxidative stress, production and/or action of hormones, growth factors and/or cytokines, and generation and activity of opposing vasoconstrictors. Considering recent advances in the field of vascular biology and diabetes, the emphasis in this review is placed on the mechanisms of hyperglycemia-induced endothelial dysfunction in the pathophysiology of diabetes-associated ED.
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