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A Cross Talk between the Endocannabinoid System and Different Systems Involved in the Pathogenesis of Hypertensive
1Department of Pharmacy Practice, College of Pharmacy, University of Hafr Al Batin, Hafr Al Batin 39524, Saudi Arabia.
Insights
The endocannabinoid system (ECS) counterbalances blood pressure and protects against hypertensive retinopathy. Upregulating the ECS or reducing vasoconstrictors like catecholamines and angiotensin II helps maintain eye health and control blood pressure.
Area of Science:
- Physiology
- Endocrinology
- Ophthalmology
Background:
- Hypertension causes organ damage, including hypertensive retinopathy, driven by factors like oxidative stress, inflammation, and vasoconstrictors from the renin-angiotensin aldosterone system (RAAS) and autonomic nervous system (ANS).
- While the roles of the RAAS and ANS in retinopathy and blood pressure regulation are known, the endocannabinoid system's (ECS) involvement remains under-explored.
- The ECS, a master regulator of bodily functions, comprises endogenous cannabinoids, degrading enzymes, and receptors influencing various organs.
Purpose of the Study:
- To review the role of the ECS in the pathogenesis of hypertensive retinopathy.
- To examine the involvement of the RAAS and ANS in hypertensive retinopathy.
- To explore the crosstalk between the ECS, RAAS, and ANS in hypertensive retinopathy.
Main Methods:
- Literature review analyzing the physiological roles and interactions of the ECS, RAAS, and ANS in blood pressure and retinopathy.
- Examination of pathways involving vasoconstrictors (catecholamines, Angiotensin II) and vasodilators (ECS) in hypertensive retinopathy.
- Analysis of how the ECS counteracts or modulates pathways influenced by the RAAS and ANS.
Main Results:
- The ECS acts as a vasodilator, counterbalancing the vasoconstrictive effects of the ANS and Angiotensin II (Ang II).
- The ECS can independently counteract vasoconstriction or block shared pathways involved in blood pressure and eye function regulation.
- Hypertensive retinopathy involves oxidative stress, ischemia, endothelial dysfunction, inflammation, and activated RAS and catecholamines.
Conclusions:
- Persistent blood pressure control and normal eye function are maintained by reducing systemic catecholamines and Ang II, or by upregulating the ECS.
- Upregulation of the ECS promotes the regression of hypertension-induced retinopathy.
- Understanding the interplay between ECS, RAAS, and ANS is crucial for managing hypertensive retinopathy.
Abstract:
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.
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