June 2015
Volume 56, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2015
Evaluation of Molecular Mechanism of Retinal Neurovascular Coupling Using Isolated 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
  • Shinichi Otani
    Ophthalmology, Asahikawa Med University, Asahikawa, Japan
  • Akitoshi Yoshida
    Ophthalmology, Asahikawa Med University, Asahikawa, Japan
  • Footnotes
    Commercial Relationships Shinji Ono, Ono Pharmaceutical Co., Ltd. (F); Taiji Nagaoka, Ono Pharmaceutical Co., Ltd. (F); Tsuneaki Omae, None; Shinichi Otani, None; Akitoshi Yoshida, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 4415. doi:
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      Shinji Ono, Taiji Nagaoka, Tsuneaki Omae, Shinichi Otani, Akitoshi Yoshida; Evaluation of Molecular Mechanism of Retinal Neurovascular Coupling Using Isolated Porcine Retinal Arterioles. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):4415.

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

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Abstract

Purpose: Retinal vessels run through retinal nerve tissue, and as such, they are constantly influenced by various transmitters released from the nervous system. This close relationship between the nervous system and blood vessels is called “neurovascular coupling”, which is known to be involved with the maintenance of retinal microcirculation and the pathogenesis of diseases concerned with retinal blood flow disorder, including diabetic retinopathy. However, it remains unclear which transmitters released from the retinal nerve tissue influence the blood vessels in the retina. Herein, we examined whether prostaglandin E2, serine, or glutamate, which are known as vasodilatory transmitters released from the nervous system in the brain, affect the retinal arterioles.

Methods: Porcine retinal arterioles were isolated, cannulated, and pressurized without flow in vitro. Diameter changes were recorded using microscopic video techniques.

Results: Prostaglandin E2 induced dose-dependent vasodilation of the retinal arterioles. The highest concentration (0.3 µM) elicited approximately 80% of the maximal dilation. In contrast, serine and glutamate did not alter the vessel diameter (P > 0.05). Furthermore, co-administration of serine and glutamate also did not affect the vessel diameter (P > 0.05).

Conclusions: Prostaglandin E2 is a transmitter released from astrocytes which induces vasodilation of the retinal arterioles in a dose-dependent manner. The current finding suggests that prostaglandin E2 released from retinal neuronal tissue may be involved with the maintenance of retinal blood flow.

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