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

Ecaterina Pavlovschi, Valeriana Pantea, Djina Borovic, Olga Tagadiuc
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Abstract

Objective: 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.

Methods: 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.

Results: 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.

Discussion: 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.

Conclusion: 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.

Abstract Image

血管紧张素II和血管紧张素转换酶:高血压视网膜病变发病机制的关键参与者。
目的:探讨高血压视网膜病变(HR)与肾素-血管紧张素系统(RAS)成分,特别是血管紧张素II (Ang II)和血管紧张素转换酶(ACE)的关系,作为高血压视网膜病变诊断和预后的潜在生物标志物。方法:共纳入90例主要诊断为高血压的患者。根据keith - wagner - barker分类将HR分为三个严重程度组。从每位参与者身上收集配对血清和泪液样本,测量Ang II和ACE水平,评估全身和眼部变化。统计分析包括正态性和方差检验,以及适当的非参数方法。A p值结果:血清Ang II水平随着HR的进展而显著升高(p=0.039),与轻度HR相比,中度HR升高42%,重度HR增加18%。撕裂Ang II水平从轻度到中度HR (p=0.022)和从轻度到重度HR (p=0.028)显著下降。随着HR的进展,血清ACE水平显著升高(p=0.032),轻度HR和中度HR之间显著升高(66%,p=0.009),而泪液ACE水平无显著差异。讨论:我们的研究结果显示,血清Ang II和ACE水平随着HR严重程度的升高而升高,表明全身RAS激活,而撕裂Ang II降低,表明局部调节改变。这些对比趋势反映了组织特异性RAS活性,并支持Ang II作为HR进展的生物标志物的潜力。泪液ACE水平不变意味着眼表受累有限。总的来说,这些数据强调了RAS成分在高血压视网膜病变中的诊断相关性和治疗潜力。结论:这些结果提示血清中Ang II水平(升高)和泪液中Ang II水平(降低)与HR严重程度相关,而ACE仅在血清中有显著变化。需要进一步的研究来阐明RAS在HR病理生理中的作用,并探索其作为眼病治疗靶点的潜力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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