Abstract
Purpose:
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.
Methods:
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.
Results:
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.
Conclusions:
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.
Keywords: 498 diabetes •
617 nitric oxide