Renin–Angiotensin–Aldosterone System (RAAS)

Overview

• RAAS is a hormonal system that regulates blood pressure.
• It provides long-term regulation of blood pressure compared to the baroreflex, which is a short-term response.

Key Components and Functions

Juxtaglomerular Cells

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

Renin

• An enzyme released into the blood.
• Converts angiotensinogen (produced by the liver) into angiotensin I.

Angiotensin I

• A peptide of 10 amino acids.
• Converted into angiotensin II by the angiotensin-converting enzyme (ACE).

Angiotensin-Converting Enzyme (ACE)

• Predominantly found in the lungs and kidneys.
• Converts angiotensin I into angiotensin II.

Angiotensin II

• An 8-amino acid peptide hormone.
• Binds to angiotensin II receptors, exerting various effects:
  • Kidneys: Promotes sodium reabsorption in the proximal convoluted tubules.
  • Systemic Arterioles: Stimulates vasoconstriction.
  • Adrenal Cortex: Induces aldosterone release, promoting sodium and water retention.
  • Central Nervous System:
    • Stimulates thirst via the hypothalamus.
    • Triggers antidiuretic hormone release from the posterior pituitary.
    • Reduces baroreceptor sensitivity to increased blood pressure, preventing counteraction of RAAS.
• Leads to increased blood volume and blood pressure.
• Short-lived, with a half-life of 1-2 minutes.
• Degraded into angiotensin III and IV, which have lesser effects.

Clinical Relevance

• Overactive or inappropriately activated RAAS can cause hypertension.
• Targeted by anti-hypertensive drugs, including:
  • ACE Inhibitors
  • Angiotensin Receptor Blockers