Certain features of will be down for maintenance the evening of Friday August 18th starting at 8:00 pm CDT until Saturday August 19th at 12:01 pm CDT.   Please note that you still have telephone and email access to our local offices. We apologize for any inconvenience.


Angiotensin is the peptide-hormonal component of the rennin-angiotensin-aldosterone system (RAAS.) As its name implies, angiotensin’s primary effect is to raise blood pressure. When the juxtaglomerular apparatus in the kidney detects a decrease in blood pressure or blood volume, it secretes the proteolytic enzyme renin. Renin specifically cleaves the globulin angiotensinogen to produce angiotensin I, a non-vasoconstrictive peptide of ten amino acids. It is a putative neurotransmitter. Angiotensin converting enzyme (ACE) cleaves away the two carboxyl-terminal amino acid residues to produce active angiotensin II. Not only does angiotensin II directly cause arteriolar vasoconstriction and renal tubule retention of sodium and water, but it also promotes aldosterone secretion by the adrenal cortex and anti-diuretic hormone by the pituitary. When the carboxy-terminal phenylalanine is cleaved from angiotensin II by ACE or other enzymes, the resulting angiotensin (1-7) acts to lower blood pressure and reduce blood volume. We offer human angiotensinogen and its multiple cleavage products. Peptide antagonists to pressor effects include saralasin and [Sar1,Thr8]-angiotensin II, while the potent receptor agonist CGP-42112A is a peptide analog with modified amino acids.