Lecture Notes: Renin-Angiotensin-Aldosterone System (RAAS)

Overview

Purpose of RAAS: Manages blood pressure, particularly when it drops.
Main Goal: Activate and utilize angiotensin II to increase blood pressure through vasoconstriction and increased blood volume.

Renin
- Released by juxtaglomerular (JG) cells in the kidneys when blood pressure drops.
- Initiates the RAAS sequence.
Angiotensinogen
- Found in the liver, activated by renin to become angiotensin I.
Angiotensin I
- Precursor to angiotensin II, requires conversion.
Angiotensin Converting Enzyme (ACE)
- Converts angiotensin I to angiotensin II.
- Located in the endothelium of lungs and kidneys.
Angiotensin II
- Active vasoconstrictor, increasing systemic vascular resistance.
- Stimulates aldosterone and ADH release.
Aldosterone
- Released from the adrenal cortex.
- Promotes sodium and water retention by kidneys, increases blood volume, decreases potassium.
Antidiuretic Hormone (ADH/ Vasopressin)
- Released by the pituitary gland.
- Causes kidneys to retain water, increasing blood volume.

Blood Pressure Drop: Triggers the sympathetic nervous system and JG cells.
Renin Release: Activates angiotensinogen to angiotensin I.
ACE Action: Converts angiotensin I to II.
Effects of Angiotensin II:
- Vasoconstriction: Narrowing blood vessels increases blood pressure like constricting a garden hose.
- Blood Volume Increase: Through aldosterone and ADH-induced retention of sodium and water.

ACE Inhibitors: Medications that lower blood pressure by inhibiting ACE, preventing the formation of angiotensin II.

RAAS Activation:
- Starts with a blood pressure drop → SNS stimulation.
- JG cells release renin → Angiotensinogen activates to angiotensin I.
- ACE converts angiotensin I to II → Vasoconstriction and increased blood volume.
- Results in increased blood pressure.