Editing ACE inhibitor (section)

===Renin–angiotensin–aldosterone system===
{{Main|Renin–angiotensin system}}
[[Image:Renin-angiotensin-aldosterone system.svg|thumb|475px|class=skin-invert-image|[[Renin–angiotensin system|Renin–angiotensin–aldosterone system]]]]
The renin–angiotensin–aldosterone system is a major blood pressure regulating mechanism. Markers of electrolyte and water imbalance in the body such as [[hypotension]], low [[Distal convoluted tubule|distal tubule]] [[Sodium in biology|sodium]] concentration, decreased blood volume and high [[sympathetic nervous system|sympathetic]] tone trigger the release of the enzyme [[renin]] from the cells of [[juxtaglomerular apparatus]] in the kidney.{{citation needed|date=August 2024}}

Renin activates a circulating liver derived [[prohormone]] [[angiotensin]]ogen by proteolytic cleavage of all but its first ten [[amino acid]] residues known as [[angiotensin I]]. [[Angiotensin converting enzyme|ACE]] (angiotensin converting enzyme) then removes a further two residues, converting angiotensin I into [[angiotensin II]]. ACE is found in the [[pulmonary circulation]] and in the [[endothelium]] of many blood vessels.<ref>Human Physiology, Silverthorn (Pearson Benjamin Cummings 2004){{Page needed|date=September 2010}}</ref> The system increases blood pressure by increasing the amount of salt and water the body retains, although angiotensin II is also a potent [[vasoconstrictor]].<ref name="Weir 1999 pp. 205–213">{{cite journal | vauthors = Weir MR, Dzau VJ | title = The renin-angiotensin-aldosterone system: a specific target for hypertension management | journal = American Journal of Hypertension | volume = 12 | issue = 12 Pt 3 | pages = 205S–213S | date = December 1999 | pmid = 10619573 | doi = 10.1016/s0895-7061(99)00103-x | publisher = Oxford University Press (OUP) }}</ref>