aliases:
- RAAS
- Renin-Angiotensin-Aldosterone-System
Renin
The juxtaglomerular cells of the glomerulus sense the sodium concentration in the glomerulus and produce renin. Renin secretion is mainly influenced by three factors:
- The juxtaglomerular apparatus, composed of juxtaglomerular cells + macula densa + mesangial cells. When renal perfusion is low, the juxtaglomerular cells sense blood pressure drop, and pressure receptors activate the juxtaglomerular cells.
- Sympathetic nerve excitation, catecholamines enter the blood and activate β1 receptors on the juxtaglomerular cells.
- The macula densa senses low sodium in the urine and transmits signals to the juxtaglomerular cells (a sudden shift from a high-sodium diet to a low-sodium diet can also stimulate renin secretion, eventually raising blood pressure).
Angiotensin-Converting Enzyme (ACE)
After renin enters the blood, it converts angiotensinogen secreted by the liver into angiotensin I.
There is a large amount of ACE in the pulmonary capillary endothelium and kidneys, which converts angiotensin I into angiotensin II, which has extensive effects:
- Activates angiotensin type I receptors leading to vasoconstriction (other receptors leading to vasoconstriction include α1, V1, ET receptors).
- Increases sympathetic nervous output, indirectly causing vasoconstriction.
- ACE can be inhibited by [[angiotensin-converting enzyme inhibitors]] produced in the lungs.
Angiotensin
Further converted into other types of angiotensin, acting on AT1 receptors (AT2 receptor antagonist):
- Causes vasoconstriction.
- Causes constriction of afferent arterioles in the kidney, reducing glomerular blood flow.
- Increases aldosterone, enhancing water and sodium reabsorption in the distal tubules and collecting ducts.
- Acts on the hypothalamus to secrete antidiuretic hormone (ADH).
Physiological Process
- Secretion of renin:
- When the afferent arteriole flow decreases (due to low blood pressure, renal artery stenosis, etc.), the juxtaglomerular cells (granular cells) of the afferent arteriole sense this and release renin.
- The macula densa of the distal tubule senses decreased sodium ion concentration and sends signals prompting the juxtaglomerular cells to release renin.
- Sympathetic nerve excitation.
- Renin converts angiotensinogen produced by the liver into angiotensin I.
- Angiotensin I passes through the lungs and is converted by ACE produced in the lungs into angiotensin II.
- Angiotensin II has two types of receptors:
- AT1 (main AT receptor in adults), activation produces strong vasoconstriction.
- AT2 (main AT receptor in children), activation causes vasodilation.
The final effects are:
- Systemic vasoconstriction (mainly small vessels), increasing blood pressure.
- Constriction of the efferent arteriole, increasing glomerular filtration rate, increasing sodium concentration, enhancing water reabsorption, raising blood pressure.
- Angiotensin II stimulates the adrenal cortex to release aldosterone, promoting potassium excretion and sodium and water retention, increasing plasma volume.
- Angiotensin II stimulates the hypothalamus and pituitary to release antidiuretic hormone, promoting water reabsorption.
Pharmacological Actions
- Prils (-pril), ACE inhibitors.
- Sartans (-sartan), angiotensin receptor blockers (ARBs).