RENIN-ANGIOTENSIN SYSTEM IN HYPERTENSION

Renin-Angiotensin System in Hypertension

Renin-Angiotensin System in Hypertension

In recent decades, our understanding of the renin-angiotensin-aldosterone system (RAAS) and agents that interrupt has undergone significant changes. Previous studies have shown that increased activation of RAAS is associated with increased risk of adverse clinical outcomes. In addition, the endpoint of basic tests, pharmacologic agents that block the RAAS, including angiotensin-converting enzyme (ACE) inhibitors, blockers, angiotensin receptor blockers (ARBs) and angiotensin-mineralocorticoid receptor (MRA) were the mainstay of antihypertensive therapy in high-risk groups including patients with myocardial infarction, heart failure and chronic renal failure. (Vassallo, 2005, 1574)

SRA, seems to be the circulation system of three components: the renin excreted by the kidneys, liver and angiotensinogen-converting enzyme (ACE) in the lungs, allowing the synthesis of angiotensin II, a system of active elements, whose effects are mediated primarily by AT 1 receptors.

Opening of the tissue RAS, as well as understanding their role in the pathophysiology of atherosclerosis and vascular remodeling have made significant progress. In recent years, basic research showed that some or all of the RAS may be present in many tissues. converting enzyme is located on the surface of endothelial cells of blood vessels and renin can be isolated in the vascular wall. Several tissues express the mRNA of renin, angiotensinogen and angiotensin-converting enzyme inhibitors: the brain, blood vessels, kidneys and heart. These results are in full support of the SRA in the same organ. Thus, it was revealed the existence of specific brain RAS), similar to RAS DEVICE RAS participates in the pathophysiology of cardiovascular disease (hypertension, atherosclerosis), and cerebral complications. (Pepine, Handberg, 2003, 16)

Renin-angiotensin cascade exists not only as a system, but generally in different tissues and organs and systems that operate independently, including the brain. , Cascade begins with the separation of angiotensinogen in the decapeptide angiotensin I (Ang I) under the action of renin. angiotensin-converting enzyme (ACE) then converts Ang I to the octapeptide activemoiety angiotensin II (AT II), whichmediates many effects, including activation of sympathetic tone, increased blood pressure vasoconstriction, vasopressin release, the effects of behavior, and so on, its type 2 angiotensin -II 1 (AT 1) and angiotensin II type 2 (K2). Several studies have shown that all components of the renin-angiotensin system (RAS) in the brain and its changes in diseases such as hypertension, stroke, Alzheimer's disease, depression, stress, memory and learning. Studies have also established the role, for example, in spontaneously hypertensive rats, the increase in brain angiotensinogen messenger RNA (mRNA) was shown to precede development of hypertension. (Davis, Furberg, 2004, 46) transgenic mice with small interfering RNA-mediated changes in various components of the RAS have shown changes in blood pressure, suggesting a causal role of this system in the pathogenesis of hypertension. Epidemiological studies in humans and experimental animal studies have shown that lack of prenatal maternal protein may lead to the development of hypertension, stroke, depression, schizophrenia, obesity, diabetes and other conditions in offspring. In addition, changes in RAS has been shown that participation in the programming of the fetus due to maternal ...