April 2014
Volume 55, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2014
Dipeptidyl Peptidase-4 Impairs Endothelial-Dependent Relaxation of Porcine Retinal Arterioles
Author Affiliations & Notes
  • Shinji Ono
    Ophthalmology, Asahikawa Med University, Asahikawa, Japan
  • Taiji Nagaoka
    Ophthalmology, Asahikawa Med University, Asahikawa, Japan
  • Tsuneaki Omae
    Ophthalmology, Asahikawa Med University, Asahikawa, Japan
  • Takayuki Kamiya
    Ophthalmology, Asahikawa Med University, Asahikawa, Japan
  • Shinichi Otani
    Ophthalmology, Asahikawa Med University, Asahikawa, Japan
  • Akitoshi Yoshida
    Ophthalmology, Asahikawa Med University, Asahikawa, Japan
  • Footnotes
    Commercial Relationships Shinji Ono, None; Taiji Nagaoka, None; Tsuneaki Omae, None; Takayuki Kamiya, None; Shinichi Otani, None; Akitoshi Yoshida, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science April 2014, Vol.55, 4347. doi:
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      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.

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      © ARVO (1962-2015); The Authors (2016-present)

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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  
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