Alswailmi Farhan Khashim
Department of Pharmacy Practice, College of Pharmacy, University of Hafr Al Batin, Hafr Al Batin 39524, Saudi Arabia.
Pharmaceuticals (Basel). 2023 Feb 23;16(3):345. doi: 10.3390/ph16030345.
The prognosis of hypertension leads to organ damage by causing nephropathy, stroke, retinopathy, and cardiomegaly. Retinopathy and blood pressure have been extensively discussed in relation to catecholamines of the autonomic nervous system (ANS) and angiotensin II of the renin-angiotensin aldosterone system (RAAS) but very little research has been conducted on the role of the ECS in the regulation of retinopathy and blood pressure. The endocannabinoid system (ECS) is a unique system in the body that can be considered as a master regulator of body functions. It encompasses the endogenous production of its cannabinoids, its degrading enzymes, and functional receptors which innervate and perform various functions in different organs of the body. Hypertensive retinopathy pathologies arise normally due to oxidative stress, ischemia, endothelium dysfunction, inflammation, and an activated renin-angiotensin system (RAS) and catecholamine which are vasoconstrictors in their biological nature. The question arises of which system or agent counterbalances the vasoconstrictors effect of noradrenaline and angiotensin II (Ang II) in normal individuals? In this review article, we discuss the role of the ECS and its contribution to the pathogenesis of hypertensive retinopathy. This review article will also examine the involvement of the RAS and the ANS in the pathogenesis of hypertensive retinopathy and the crosstalk between these three systems in hypertensive retinopathy. This review will also explain that the ECS, which is a vasodilator in its action, either independently counteracts the effect produced with the vasoconstriction of the ANS and Ang II or blocks some of the common pathways shared by the ECS, ANS, and Ang II in the regulation of eye functions and blood pressure. This article concludes that persistent control of blood pressure and normal functions of the eye are maintained either by decreasing systemic catecholamine, ang II, or by upregulation of the ECS which results in the regression of retinopathy induced by hypertension.
高血压的预后会通过引发肾病、中风、视网膜病变和心脏肥大导致器官损害。视网膜病变与血压已围绕自主神经系统（ANS）的儿茶酚胺和肾素-血管紧张素-醛固酮系统（RAAS）的血管紧张素II进行了广泛讨论，但关于内源性大麻素系统（ECS）在视网膜病变和血压调节中的作用却鲜有研究。内源性大麻素系统（ECS）是体内一个独特的系统，可被视为身体功能的主要调节者。它包括内源性大麻素的产生、其降解酶以及在身体不同器官中支配并执行各种功能的功能性受体。高血压性视网膜病变通常是由于氧化应激、缺血、内皮功能障碍、炎症以及具有血管收缩生物学特性的肾素-血管紧张素系统（RAS）和儿茶酚胺激活所致。那么问题来了，在正常个体中，是哪个系统或物质能抵消去甲肾上腺素和血管紧张素II（Ang II）的血管收缩作用呢？在这篇综述文章中，我们讨论了ECS的作用及其对高血压性视网膜病变发病机制的贡献。这篇综述文章还将研究RAS和ANS在高血压性视网膜病变发病机制中的参与情况以及这三个系统在高血压性视网膜病变中的相互作用。这篇综述还将解释，作为血管舒张剂的ECS，要么独立抵消由ANS和Ang II血管收缩产生的效应，要么阻断ECS、ANS和Ang II在调节眼功能和血压时共有的一些常见途径。本文得出结论，持续控制血压和维持眼睛的正常功能，要么通过降低全身儿茶酚胺、Ang II来实现，要么通过上调ECS来实现，这会导致高血压诱导的视网膜病变消退。
