RAS peptides

The renin-angiotensin-aldosterone system (RAAS) is a critical regulator of plasma sodium concentration, arterial blood pressure and extracellular volume in a systemic manner in response to chronic changes. RAAS, often shortened to RAS, has three main functional proteins: renin, angiotensin II, and aldosterone. RAS can be activated by decreased renal blood pressure, decreased plasma sodium concentration to the distal convoluted tubule or beta-agonism action.

Activation of RAS leads to renin release from the juxtaglomerular kidney cells to hydrolyse angiotensinogen to angiotensin I. Angiotensin I is converted to angiotensin II by angiotensin-converting enzymes (ACE) in the vascular epithelium, primarily in the lungs. The binding of angiotensin II binds to its AT receptors and increases aldosterone levels causing vasoconstriction and increased sodium absorption in the proximal tubule. This causes an increase in blood volume and blood pressure. Additionally, angiotensin triggers thirst sensation in the hypothalamus for increased water intake and vasopressin release leading to more significant water reabsorption by inserting aquaporin in the kidney collection ducts.

RAS can alleviate chronic changes in blood pressure and vascular resistance through these mechanisms. RAS function can be vital, but inappropriate activation has been linked to numerous clinical conditions, including hypertension, heart failure and diabetes.