Renin–Angiotensin–Aldosterone System (RAAS)

Overview

• RAAS is a hormonal system that regulates blood pressure over the long term.
• Unlike baroreflex, which is a short-term response, RAAS manages sustained blood pressure control.

Components of RAAS

Juxtaglomerular Cells

• Located in the kidneys, within the walls of afferent arterioles.
• Produce prorenin, which upon activation by low blood pressure, is converted to renin.

Renin

• Released into the blood, converts angiotensinogen (from the liver) into angiotensin I (10 amino acids).

Angiotensin I to Angiotensin II Conversion

• Angiotensin I is converted to Angiotensin II (8 amino acids) by ACE (angiotensin-converting enzyme).
• ACE is primarily found in the lungs and kidneys.

Functions of Angiotensin II

• Sodium Reabsorption: Promotes reabsorption in proximal convoluted tubules of the kidneys.
• Vasoconstriction: Stimulates vasoconstriction in systemic arterioles.
• Aldosterone Release: Induces release from the adrenal cortex, leading to sodium and water retention in kidneys.
• Central Nervous System Effects:
  • Stimulates thirst via the hypothalamus.
  • Promotes ADH (antidiuretic hormone) release from the posterior pituitary, aiding water retention.
  • Reduces baroreceptor sensitivity to high blood pressure, preventing interference with RAAS.

Outcomes

• These actions increase blood volume and blood pressure.
• Angiotensin II is short-lived (half-life 1-2 minutes).
• Degraded into angiotensin III and IV, with lesser effects.

Clinical Relevance

• Hypertension: Overactive or inappropriate RAAS activation can cause hypertension.
• Treatment: RAAS is a target for anti-hypertensive drugs.
  • ACE Inhibitors
  • Angiotensin Receptor Blockers

RAAS plays a crucial role in maintaining blood pressure and is a key target in treating hypertension.