THE CORRELATION BETWEEN THE RENIN AT ALDOSTERONE SYSTEM - ARTERIAL HYPERTENSION AND HORMONAL MECHANISMS

The aim of this study was to evaluate the effect of the renin- angiotensin- aldosterone system on blood pressure from a hormonal perspective. Additionally, the correlation between cardiovascular pathology and the mechanisms of this system was examined. Material and methods. A comprehensive literature search was conducted using databases such as PubMed, MEDLINE, and Cochrane Library, focusing on studies related to hormonal mechanisms in hypertension and the renin- angiotensin -aldosterone system. Data extraction and quality assessment were performed on relevant peer-reviewed articles, clinical trials, cohort studies, and meta-analyses. Results and discussions. The study indicates that the etiology of hypertension cannot be attributed to a single, identifiable cause in more than 90% of cases. Numerous mechanisms are involved, including genetic predisposition, vascular remodeling, endothelial dysfunction, renal water and salt retention, dysfunction of the renin- angiotensin -aldosterone system, sympathetic autonomic hypertension, and insulin resistance. These mechanisms are frequently associated with factors for high blood pressure such as obesity, a sedentary lifestyle, increased salt consumption, dyslipidemia, and increased alcohol consumption. The key element in the hormonal mechanisms is the renin- angiotensin -aldosterone system, which is primarily responsible for water retention and increased blood pressure. High blood pressure is a major cardiovascular risk factor with an increasing incidence in the elderly population. However, angiotensin II can also be produced at the tissue level independently of the converting enzyme, significantly contributing to the onset and progression of hypertension and ventricular hypertrophy. Conclusions: The studies illustrate the activation of the renin- angiotensin- aldosterone system in prehypertensive subjects and highlight the benefits of early pharmacological intervention to limit the actions of angiotensin II, thereby delaying the progression to high blood pressure.