RENIN - ANGIOTENSIN - ALDOSTERONE SYSTEM
Dr. David Lyness
Surface of pulmonary endothelium
Surface of renal endothelium
Decrease in renal perfusion via the Juxtaglomerular Apparatus
Tubular Sodium + Chloride reabsorption.
FIGHT OR FLIGHT
Produced in the adrenal cortex
and increase in BP
from posterior pituitary
from collecting duct
More water and salt in blood, increases
and improves JGA perfusion
RENIN - Made in JGA - stimulated by raised sympathetic tone, falling plasma volume, and prostaglandins (PGE2)
ANGIOTENSIN 2 - Also increases tone in the efferent glomerular arteriole. This leads to an increased filtration fraction, & increases sodium reabsorption
ALDOSTERONE - Release is also potentiated by hyperkalaemia. Acts on the distal tubule and causes sodium reabsorption that then facilitates water re-abs.
ADH - Causes passive absorption of water from the collecting ducts, concentrating the urine - (holds on to water). Surgical stimuli causes ADH secretion.
ANP - Atrial Natriuretic Peptide - increases sodium loss by increasing GFR and blocking sodium reabsorption from the proximal collecting duct
You can now see how ACEI, ARB's, Aldosterone Antagonists and even diuretics can alter BP
Positive stimulation of the RAAS system can increase BP
Controlling Fluid & Salt Homeostasis