May 2003
Volume 44, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2003
Angiotensin II Modulates Electroretinogram (ERG) Amplitudes but Not Implicit Times in vivo
Author Affiliations & Notes
  • J. Takahashi
    Eye Research, Joslin Diabetes Center, Boston, MA, United States
  • A. Clermont
    Eye Research, Joslin Diabetes Center, Boston, MA, United States
  • H. Salti
    Eye Research, Joslin Diabetes Center, Boston, MA, United States
  • D. Bursell
    Eye Research, Joslin Diabetes Center, Boston, MA, United States
  • N. Horio
    Department of Ophthalmology, Nagoya University, Nagoya, Japan
  • S.E. Bursell
    Department of Ophthalmology, Nagoya University, Nagoya, Japan
  • Footnotes
    Commercial Relationships  J. Takahashi, None; A. Clermont, None; H. Salti, None; D. Bursell, None; N. Horio, None; S.E. Bursell, None.
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 1874. doi:
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      J. Takahashi, A. Clermont, H. Salti, D. Bursell, N. Horio, S.E. Bursell; Angiotensin II Modulates Electroretinogram (ERG) Amplitudes but Not Implicit Times in vivo . Invest. Ophthalmol. Vis. Sci. 2003;44(13):1874.

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

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Abstract

Abstract: : Purpose: The renin-angiotensin system ( RAS) is activated in diabetes and has been correlated with risk for diabetic retinopathy development. The inhibition of angiotensin converting enzyme ( ACE) and its receptor blockade suggest that angiotensin adversely effects the ERG response. In this study, we investigate the direct role of angiotensin upon the ERG. Methods: C57BL/6 mice were used in this study. Jugular catheters were inserted 24 hours prior to measurements. Angiotensin II ( AII) infusions ( 120µl of 7.5mg/ml AII) or saline alone were performed for 2 hours in conscious animals. At one hour, animals were dark- adapted for at 60 minutes before ERG recording. Animals were anesthetized with ketamine/xylazine. A contact lens electrode was used with a single flash of 1.5x104cd/m2 ( 5msec duration) as a stimulus. Following the infusion, ERG were recorded and averaged. The peak latencies and amplitudes for the oscillatory potentials ( OP1-4) and a & b-waves were measured. Results: In the group receiving AII infusion, the amplitude for OP2 was decreased by 52±13% ( 119±30 vs 228±39µV, p = 0.045) and for the b-wave by 64±1% ( 364±7 vs 573±7µV, p = 0.023) as compared with vehicle control. Implicit times for OP1 to 4, a-wave, and b-wave tended to be prolonged in the group receiving AII infusion compared to the saline infused animals but did not reach statistical significance given the variances and the small number of animals per group studied to date. Conclusions: The function of RAS in the neuronal retina remains undetermined. Our results showed that AII decreased the amplitude for OP2 and b-wave directly. It is possible that the increased vasoconstrictive tone associated with AII increase reduced neuronal perfusion resulting in the decreased amplitudes measured here. This study indicates that AII may be implicated with some neurophysiological parameters indicative of ERG impairment in the diabetic retina.

Keywords: electroretinography: non-clinical • diabetic retinopathy • diabetes 
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