Renin Angiotensin Aldosterone System (RAAS)
Role of Renin Angiotensin Aldosterone System (RAAS)
RAAS is involved in regulation of...
Blood pressure
Blood volume
Fall in blood pressure or fall in blood volume
↓
RAAS gets activated
↓ Brings pressure and volume back to normal
Broadly, the Events During RAAS are:
Detection of fall in blood pressure or blood volume
↓
Release of renin from juxtaglomerular cells in the kidney
↓
Synthesis of angiotensin II
↓
Effects of angiotensin II
↓
Brings pressure and volume back to normal
Detection of Fall in Blood Pressure or Blood Volume & Release of Renin
There are 3 sites that can detect fall in blood pressure or blood volume:
Baroreceptors
Macula densa cells
Jusgraglomerular cells
They all eventually cause the release of renin.
Baroreceptor
are located in carotid sinus and aortic arch.
are sensitive to stretch in vessel wall.
Fall in blood pressure
↓
Decreased stretching of the vessel wall
↓
Detected by baroreceptors
↓ Send the signals via cranial nerves IX and X
↓ Signal reaches medullary control centers
↓
Increased sympathetic outflow to juxtaglomerular cells in the kidney
↓
Causes release of renin
Macula Densa Cells
are part of juxtaglomerular apparatus in kidney.
located in ascending limb of loop of Henle of renal tubule.
are sensitive to sodium (Na) concentration in the lumen of renal tubule.
Fall in blood pressure or blood volume
↓
Fall in GFR
↓
Decreased Na concentration in lumen of renal tubule at macula densa cells
↓
Detected by macula densa cells
↓
Release nitric oxide and prostaglandins
↓
Stimulate juxtaglomerular cells
↓ Release of renin
Juxtaglomerular Cells
are part of juxtaglomerular apparatus in kidney.
located in afferent arteriole of the glomerulus.
are sensitive to stretch in vessel wall.
Fall in blood pressure or blood volume
↓
Reduced stretch on vessel wall
↓
Detected by juxtaglomerular cells
↓
Release renin
Synthesis of Angiotensin II
Liver releases angiotensinogen
↓
Renin converts agntiotensionogen into angiotensin I
↓
Angiotensin Converting Enzyme (ACE) converts agniotensin I into antiotensin II
Effects of Angiotensin II
Vasoconstriction
Mainly the constriction of arterioles
↓
Increased total peripheral resistance
↓ Increased blood pressure
Constriction of veins to some extend
↓
Increased venous return
↓
Increased cardiac output
↓
Increased blood pressure
Na retention
Angiotensin increases Na retention by multiple mechanisms as follows:
Angiotensin II stimulates glomerulosa cells in adrenal cortex
↓
Release of aldosterone
↓ Aldosterone increases synthesis of proteins involved in Na reabsorption in principle cells of collecting duct
↓ Increased Na reabsorption.
...
Angiotensin II increases activity of Na-H exchanger in proximal tubule
↓
Increased reabsorption of Na.
...
Angiotensin II causes constriction of efferent arteriole
↓ 1. Decreased hydrostatic pressure in peritubular capillary.
2. Increased filtration fraction → increased colloid osmotic pressure in peritubular capillary.
↓
Increased uptake of reabsorbate from interstitum into peritubular capillary
↓ Increased reabsorption from renal tubule including that of Na and water.
...
Na retention (as explained above) → Causes water retention osmotically → Increased blood volume and blood pressure
Increase Body Water
Angiotensin II acts on hypothalamus
↓
1. Causes release of ADH from hypothalamus → Increased water reabsorption from kidney.
2. Induces thirst → increased water intake.
↓
Increase in body water
↓ Increased blood volume and blood pressure
Termination of Angiotensin II Action
Angiotensin II continues to be produced until blood pressure or volume is restored.
Half-life of angiotensin II is about 2 minutes.
It is degraded by angiotensinases.