Investigative Ophthalmology & Visual Science Cover Image for Volume 65, Issue 7
June 2024
Volume 65, Issue 7
Open Access
ARVO Annual Meeting Abstract  |   June 2024
Systemic hypertension leads to declined retinal functions via neuroinflammation related pathways
Author Affiliations & Notes
  • Yingkun Cui
    School of Optometry, The Hong Kong Polytechnic University, Hong Kong, Hong Kong
  • Li Pan
    School of Optometry, The Hong Kong Polytechnic University, Hong Kong, Hong Kong
  • Lanlan Zhang
    Department of Biomedical Engineering, The Hong Kong Polytechnic University, Hong Kong, Hong Kong
  • Manhui Wu
    School of Optometry, The Hong Kong Polytechnic University, Hong Kong, Hong Kong
  • Chunyi Wen
    Department of Biomedical Engineering, The Hong Kong Polytechnic University, Hong Kong, Hong Kong
    Research Institute of Smart Ageing (RISA), The Hong Kong Polytechnic University, Hong Kong, Hong Kong
  • Chi-wai Do
    School of Optometry, The Hong Kong Polytechnic University, Hong Kong, Hong Kong
    Research Centre for SHARP Vision (RCSV), The Hong Kong Polytechnic University, Hong Kong, Hong Kong
  • Footnotes
    Commercial Relationships   Yingkun Cui None; Li Pan None; Lanlan Zhang None; Manhui Wu None; Chunyi Wen None; Chi-wai Do None
  • Footnotes
    Support  Health Medical Research Fund (20212781); RISA (CD65); RCSV (1-BBDD); 1-WZ25
Investigative Ophthalmology & Visual Science June 2024, Vol.65, 6763. doi:
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      Yingkun Cui, Li Pan, Lanlan Zhang, Manhui Wu, Chunyi Wen, Chi-wai Do; Systemic hypertension leads to declined retinal functions via neuroinflammation related pathways. Invest. Ophthalmol. Vis. Sci. 2024;65(7):6763.

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

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Abstract

Purpose : The relationship between systemic hypertension (HT) and the incidence of glaucoma, as well as the underlying mechanism responsible for the HT-induced ocular changes, remain elusive. In this study, we investigated the longitudinal changes of intraocular pressure (IOP) profile and functional retinal responses at different stages of HT.

Methods : Stroke-prone spontaneously hypertensive rats (SHR) were used as the animal model of primary hypertension. Wistar-Kyoto rats (WKY) were used as the normotensive control animals. Measurements of IOP and functional retinal response were conducted by a rebound tonometer and full-field electroretinogram (ERG), respectively. Longitudinal monitoring of blood pressure (BP), IOP and ERG response were conducted at 4, 8, and 12 months for both species. Retinas of 12-month SHR and WKY were collected for qPCR and RNA-sequencing studies.

Results : Systolic BP was substantially higher in SHR compared to the age matched WKY at all time points measured (N=9 for SHR, N=9 for WKY, two-way ANOVA with Bonferroni's multiple comparisons test, P<0.0001). However, IOP was consistently lower in SHR compared to WKY at all time points (9.1±0.1 mmHg in SHR vs 10.6±0.1 mmHg in WKY at 4 months; 9.2±0.1 mmHg in SHR vs 10.5±0.2 mmHg in WKY at 8 months; 9.0±0.1 mmHg in SHR vs 10.6±0.2 mmHg in WKY at 12 months, P<0.0001). Using full-field ERG, no significant differences in positive scotopic threshold response (pSTR), photopic a- and b-wave were observed at 4 months. At 8 months, SHR demonstrated a 27% reduction in the amplitude of pSTR (P<0.0001) and a 19% reduction in the amplitude of a-wave (P<0.01) compared with WKY. At 12 months, the amplitudes of pSTR, a-wave, and b-wave in SHR reduced by 40% (P<0.0001), 29% (P<0.0001), and 23% (P<0.001), respectively. The qPCR analysis revealed increased expressions of Il-1β, Cd68 and Ccl2 in the retina of 12-month SHR compared with age matched WKY, while only CD68 was found to be elevated at 8 months. The RNA-sequencing findings also demonstrated increased inflammation, complement activation, and Toll-like receptor activation in the retina of 12-month SHR compared with age-matched WKY.

Conclusions : Chronic HT leads to progressively declined retinal functions. The reduction of functional responses from retinal ganglion cells and other retinal cells in SHR are triggered through IOP-independent, neuroinflammation-mediated mechanisms.

This abstract was presented at the 2024 ARVO Annual Meeting, held in Seattle, WA, May 5-9, 2024.

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