page_title: Angiotensin
section_title: Angiotensin I
hierarchical_section_title: Angiotensin / Precursor and types / Angiotensin I
caption_attribution_description: English: The renin-angiotensin system (RAS) or the renin-angiotensin-aldosterone system (RAAS). Start reading this schematic from the left, where it says "Decrease in renal perfusion (juxtaglomerular apparatus)". Alternatively, the RAAS can also be activated by a low NaCl concentration in the macula densa or by sympathetic activation. Legend info: Blue and red dashed arrows indicate stimulatory or inhibitory signals, which is also indicated by the +/-. In the tubule and collecting duct graphics, the grey dashed arrows indicate passive transport processes, contrary to the active transport processes which are indicated by the solid grey arrows. The other solid arrows either indicate a secretion from an organ (blue, with a starting Spot) or a reaction (black). These 2 processes can be stimulated or inhibited by other factors.
context_page_description: Angiotensin is a peptide hormone that causes vasoconstriction and an increase in blood pressure. It is part of the renin–angiotensin system, which regulates blood pressure. Angiotensin also stimulates the release of aldosterone from the adrenal cortex to promote sodium retention by the kidneys.
  An oligopeptide, angiotensin is a hormone and a dipsogen. It is derived from the precursor molecule angiotensinogen, a serum globulin produced in the liver. Angiotensin was isolated in the late 1930s and subsequently characterized and synthesized by groups at the Cleveland Clinic and Ciba laboratories.
context_section_description: Asp-Arg-Val-Tyr-Ile-His-Pro-Phe-His-Leu | Val-Ile-...
  Angiotensin I (CAS# 11128-99-7), officially called proangiotensin, is formed by the action of renin on angiotensinogen. 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 ) at the juxtaglomerular cells, or decreased delivery of Na+ and Cl- to the macula densa.  If a reduced NaCl concentration in the distal tubule is sensed by the macula densa, renin release by juxtaglomerular cells is increased. This sensing mechanism for macula densa-mediated renin secretion appears to have a specific dependency on chloride ions rather than sodium ions. 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. This, and similar findings obtained in vivo, 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 I appears to have no direct biological activity and exists solely as a precursor to angiotensin II.
caption: Renin–angiotensin–aldosterone system
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