Angiotensin II is the biologically active product of renin " “angiotensin system. It is an oligopeptide of eight amino acids and very strong physiologic vasoconstrictor. The concentration of ACE is highest in the lung, and it had been thought that most angiotensin II formation occurred in the pulmonary circulation. It is now clear, however, that ACE is produced in the vascular endothelium of many tissues; therefore, angiotensin II can be synthesized at a variety of sites, including the kidney, vascular endothelium, adrenal gland, and brain.
Alternative enzymatic pathways not involving ACE may contribute to angiotensin II production. Angiotensin II binds to its specific receptors and exerts its effects in the brain, kidney, adrenal, vascular wall, and the heart. The actions of circulating angiotensin II contribute to hypertension. This may indirectly influence cardiac function, irrespective of any direct effect on the heart and myocardium.
Circulating angiotensin II promotes sodium and water reabsorption, increasing intravascular fluid volume, which in turn increases cardiac preload and, therefore, stroke volume. Circulating angiotensin II causes systemic arteriolar vasoconstriction, thereby increasing vascular resistance and cardiac afterload. Angiotensin II also affects the autonomic nervous system, stimulating the sympathetic nervous system and reducing vagal activity. These actions are oriented toward maintaining the blood pressure when the renin " “angiotensin system is activated by effective volume depletion.
Normal range: 10 " “60 pg/mL.
Use
Evaluating hypertension
Interpretation
Increased In
Hypertension
Renin-secreting juxtaglomerular renal tumor
Volume depletion
CHF
Decreased In
Anephric patients
Primary aldosteronism
Cushing syndrome
Limitations
Patient should be on normal-sodium diet and be recumbent for 30 minutes before specimen collection.
Short lived in plasma (half-life is 5 minutes) degraded into inactive peptides, plasma should be separated and frozen immediately.