Angiotensin II and angiotensin converting enzyme: key players in the pathogenesis of hypertensive retinopathy

TL;DR

This study explores how angiotensin II and ACE levels in blood and tears relate to the severity of hypertensive retinopathy, suggesting their potential as biomarkers.

Contribution

The study identifies contrasting trends in serum and tear levels of Ang II and ACE in relation to HR severity, highlighting their potential as biomarkers.

Findings

Serum Ang II and ACE levels increase with the severity of hypertensive retinopathy.

Tear Ang II levels decrease as HR severity increases, indicating altered local RAS regulation.

Tear ACE levels remain unchanged, suggesting limited ocular surface involvement in HR.

Abstract

To investigate the association between hypertensive retinopathy (HR) and components of the renin-angiotensin system (RAS), specifically angiotensin II (Ang II) and angiotensin-converting enzyme (ACE), as potential biomarkers for the diagnosis and prognosis of HR.

A total of 90 patients diagnosed primarily with hypertension were prospectively enrolled. HR was graded according to the Keith-Wagener-Barker classification into three severity groups. Paired serum and tear fluid samples were collected from each participant to measure Ang II and ACE levels, assessing both systemic and ocular changes. Statistical analyses included tests for normality and variance, as well as appropriate non-parametric methods. A p-value <0.05 was considered significant.

Serum Ang II levels increased significantly with advancing stages of HR (p=0.039), showing a 42% rise in moderate HR compared to mild HR and an additional 18% increase in severe HR. Tear Ang II levels decreased markedly from mild to moderate HR (p=0.022) and from mild to severe HR (p=0.028). Serum ACE levels rose significantly as HR progressed (p=0.032), notably between mild and moderate HR (66% increase, p=0.009), whereas tear ACE levels showed no significant differences.

Our findings showed that serum Ang II and ACE levels rise with HR severity, indicating systemic RAS activation, while tear Ang II decreases, suggesting altered local regulation. These contrasting trends reflect tissue-specific RAS activity and support the potential of Ang II as a biomarker for HR progression. The unchanged tear ACE levels imply limited ocular surface involvement. Overall, the data underscore RAS components’ diagnostic relevance and therapeutic potential in hypertensive retinopathy.

These findings suggest that Ang II levels in serum (increasing) and tears (decreasing) correlate with HR severity, while ACE changes are significant only in serum. Further studies are warranted to elucidate the role of RAS in HR pathophysiology and to explore its potential as a therapeutic target in ocular disease.

Figures