Renin Angiotensin Aldosterone System (RAAS)

Flashcards reviewing the renin angiotensin aldosterone system, its components, and clinical significance.

What is the RAAS?

The Renin Angiotensin Aldosterone System is a cascade of hormones, enzymes and proteins that regulate fluid retention and vasoconstriction.

What initiates the RAAS?

The kidneys initiate the RAAS by releasing renin in response to decreases in blood pressure or blood volume.

What causes decreases in blood pressure or blood volume that trigger the RAAS?

Dehydration, bleeding, or sodium level issues.

What is renin?

An enzyme released into bloodstream by juxtaglomerular cells in kidneys that converts angiotensinogen into angiotensin I.

Where is angiotensinogen produced?

In the liver.

What is angiotensinogen?

A glycoprotein synthesized by the liver, excreted into the bloodstream and serves as a substrate for the enzyme renin.

What are Angiotensin Converting Enzymes (ACE)?

Proteins that convert inactive peptide angiotensin I into angiotensin II, primarily found in the lungs, liver, and endothelial lining.

What is Angiotensin II?

A peptide hormone that causes vasoconstriction, stimulates release of aldosterone and antidiuretic hormone, increases thirst and sodium craving, and causes renal tubules to retain sodium and water.

What is aldosterone?

A steroid hormone produced by the adrenal cortex that promotes sodium reabsorption, increases potassium excretion, regulates blood pressure by controlling sodium and water balance, and assists acid/base balance by promoting hydrogen excretion.

What is the role of Antidiuretic Hormone (ADH) in the RAAS?

Angiotensin II stimulates ADH release from the pituitary gland, which promotes kidneys to increase water retention, increasing blood volume and blood pressure.

What is the clinical significance of the RAAS?

It is a crucial mediator of cardiac, vascular, and renal physiology through regulating vascular tone and salt and water homeostasis and plays a significant role in the pathophysiological conditions of hypertension, heart failure, other cardiovascular diseases, and renal diseases.

How can overactivation of RAAS be managed?

Blockade of the overactivation of RAAS by various medications has been shown to improve outcomes in various cardiovascular and renal diseases.