angiotensin

see also:

• renin
• aldosterone
• ACE inhibitors
• renin-angiotensin system inhibitors (RAS)

image courtesy of wikipedia

• angiotensin II is a peptide hormone that produces vasoconstriction, promotes water and salt retention, increased BP, and stimulates release of aldosterone
• circulating inactive angiotensinogen is a globulin produced by the liver and converted to inactive angiotensin I by renin
• the inactive angiotensin I is then converted to active angiotensin II by angiotensin converting enzyme (ACE) mainly within the lung but also in endothelium and renal epithelium
• angiotensin converting enzyme (ACE) is blocked by ACE inhibitors
• angiotensin II has a half life in the circulation of ~30secs (may be up to 30 minutes in tissues) and is degraded by:
  • angiotensinases to angiotensin III which has 100% of aldosterone stimulating activity but only 40% of pressor activity
    • angiotensin III is degraded to angiotensin IV which is partly active
  • ACE2 to the vasodilator, angiotensin-(1-7)
• angiotensins act on angiotensin receptors which are blocked by angiotensin receptor blockers

• main receptor acted on by AG II
• causes vasoconstriction, aldosterone secretion, etc

• probably involved in fetal vascular growth and other tissue growth
• activated by AG II

• poorly characterized as yet

• poorly characterized as yet
• activated by AG IV
• may have roles in CNS extracellular matrix and in modulation of oxytocin release

• constricts arteries and veins and increasing blood pressure
• prothrombotic
  • stimulation of PAI-1 and PAI-2
  • increased adhesion and aggregation of platelets
• Gq stimulator of the heart causing cardiac hypertrophy
• increases thirst sensation and salt desire
• directly increases renal sodium reabsorption
• increases argipressin (vasopressin / ADH) secretion
• increases adrenocorticotropic hormone (ACTH) secretion
• potentiates the release of noradrenaline / norepinephrine
• decreases the response of the baroreceptor reflex
• increases aldosterone secretion
• complex effects on GFR and RBF
• sensitizes to tubuloglomerular feedback
• causes the local release of prostaglandins in kidney which antagonise renal vasoconstriction
• upregulates of adipose tissue lipogenesis
• downregulates lipolysis

• this vasodilator peptide generally appears to oppose the pressor, proliferative and pro-fibrotic actions of Ang II
• acts through its own G-protein-coupled receptor