الفهرس 
Overview on Reninangiotensin- Reninangiotensin- SystemOnly 14 pages are availabe for public view
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Abstract
The renin-angiotensin-aldosterone system (RAS) classically was defined as a circulating hormonal system regulating blood pressure, electrolytes and fluids homeostasis. Later on, an expanded view of RAS has gradually emerged.In the classic pathway of RAS, renin converting Angiotensinogen (AGT) to Angiotensin I (Ang I); which hydrolyzed by Angiotensin Converting Enzyme (ACE) to Angiotensin II (Ang II); a biologically active substrate playing a vital roles via different receptors as AT1 and AT2 receptors. The expanded component includes: local ‘tissue RAS’ in most organs and tissues, intracellular RAS, biologically active peptides {Angiotensin III (Ang III), Angiotensin IV (Ang IV) and Angiotensin 1-7 ( Ang 1-7), Angiotensin Converting Enzyme 2 (ACE 2) and angiotensinases.
Myocardial Infarction (MI) can be divided into two major types: subendocardial and transmural. Ventricular remodeling is regulated by mechanical, neurohormonal and genetic factors. Post-infarction remodeling has been divided into an early phase (within 72 hours) and a late phase (beyond 72hours). Increased AngII production Plays; via the AT1 receptor, a mandatory role in both phases of remodeling.
Oral Angiotensin Converting Enzyme Inhibitors (ACE-Is) are beneficial in Acute Myocardial Infarction (AMI) patients and should be administered within the first 24 hours to patients with ST segment Elevation Myocardial Infarction (STEMI) with anterior location or Heart Failure (HF) and reasonable for all patients with STEMI. Some patients couldn’t tolerate ACE-Is due to its side effects. Clinical trails on ACE-Is include: SAVE, TRACE, GISSI-3, SOLVD and PREAMI trials.
The recent guidelines document that Angiotensin Receptor Blockers (ARBs) should be given to patients with STEMI who have indications for but are intolerant of ACE-Is. Trails on ARBs include: OPTIMAAL and & VALIANT trials.
New therapeutic pathways include biased AT1-receptor blockade, AT1- receptor blockade combined with Neutral Endopeptidase (NEP) inhibition, AT1-receptor blockade combined with Nitric Oxide (NO) relasing and Ang II type 2 receptor stimulation Compound 21(C21).