[10] Obtaining actual crystals for X-ray diffractometric analysis is difficult in part due to the variability of glycosylation that angiotensinogen exhibits.

Renin cleaves the peptide bond between the leucine (Leu) and valine (Val) residues on angiotensinogen, creating the decapeptide (ten amino acid) (des-Asp) angiotensin I. Renin is produced in the kidneys in response to renal sympathetic activity, decreased intrarenal blood pressure (<90mmHg systolic blood pressure[11] ) at the juxtaglomerular cells, dehydration or decreased delivery of Na+ and Cl- to the macula densa.

[12] If a reduced NaCl concentration[13] in the distal tubule is sensed by the macula densa, renin release by juxtaglomerular cells is increased.

Studies using isolated preparations of thick ascending limb with glomerulus attached in low NaCl perfusate were unable to inhibit renin secretion when various sodium salts were added but could inhibit renin secretion with the addition of chloride salts.

[14] This, and similar findings obtained in vivo,[15] has led some to believe that perhaps "the initiating signal for MD control of renin secretion is a change in the rate of NaCl uptake predominantly via a luminal Na,K,2Cl co-transporter whose physiological activity is determined by a change in luminal Cl concentration.

Angiotensin II increases blood pressure by stimulating the Gq protein in vascular smooth muscle cells (which in turn activates an IP3-dependent mechanism leading to a rise in intracellular calcium levels and ultimately causing contraction).

Other cleavage products of ACE, seven or nine amino acids long, are also known; they have differential affinity for angiotensin receptors, although their exact role is still unclear.

Angiotensin II results in increased inotropy, chronotropy, catecholamine (norepinephrine) release, catecholamine sensitivity, aldosterone levels, vasopressin levels, and cardiac remodeling and vasoconstriction through AT1 receptors on peripheral vessels (conversely, AT2 receptors impair cardiac remodeling).

This is why ACE inhibitors and ARBs help to prevent remodeling that occurs secondary to angiotensin II and are beneficial in congestive heart failure.

It is a peptide that is formed by removing an amino acid from angiotensin II by glutamyl aminopeptidase A, which cleaves the N-terminal Asp residue.

[25][26] Synthetic small molecule analogues of angiotensin IV with the ability to penetrate through blood brain barrier have been developed.

[28] Studies have also shown that the usual biological effects of angiotensin IV on the body are not affected by common AT2 receptor antagonists such as the hypertension medication Losartan.

It has a complex and variable effect on glomerular filtration and renal blood flow depending on the setting.

Angiotensin II causes the local release of prostaglandins, which, in turn, antagonize renal vasoconstriction.