Purchase this article with an account.
Shinji Ono, Taiji Nagaoka, Tsuneaki Omae, Takayuki Kamiya, Shinichi Otani, Akitoshi Yoshida; Dipeptidyl Peptidase-4 Impairs Endothelial-Dependent Relaxation of Porcine Retinal Arterioles. Invest. Ophthalmol. Vis. Sci. 2014;55(13):4347.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
Dipeptidyl Peptidase-4 (DPP-4) is multifunctional protein playing a major role in the degradation of incretin peptide hormones which have glucose lowering effect. Recently, DPP-4 has identified as a novel adipokine releasing from adipose tissue. Furthermore, recent epidemiological studies confirm that elevated DPP-4 levels in serum are associated with type 2 diabetes, suggesting that over-production of DPP-4 might play a role in the pathogenesis of diabetic microvascular complications. However, the direct effect of DPP-4 on ocular microvascular reactivity remains unknown. Herein, we examined whether DPP-4 can affect endothelium-dependent nitric oxide (NO)-mediated dilation of retinal arterioles.
Porcine retinal arterioles were isolated, cannulated, and pressurized without flow in vitro. Diameter changes were recorded using video microscopic techniques. To evaluate the vessel endothelial function the reactivity to endothelium-dependent NO-mediated agonist bradykinin (10nM) was used. We compared the endothelial function before and after 180 minutes of intraluminal incubation with 1,000 ng/ml of DPP-4.
Intraluminal treatment with DPP-4 significantly attenuated the bradykinin-induced vasodilation to about half (P<0.05). Whereas the reactivity to the endothelium-independent NO donor sodium nitroprusside was not altered.
DPP-4 inhibits the endothelium-dependent NO-mediated dilation in retinal arterioles. By impairing endothelium-dependent NO-mediated vasoreactivity, DPP-4 can potentially facilitate the development of diabetic retinopathy.
This PDF is available to Subscribers Only