Angiotensin-Converting Enzyme: Difference between revisions

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David Canner, Alexander Berchansky, Michal Harel, Cristina Murga

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 ACE is a Zn and Chloride dependent type-1 membrane protein (N-terminal regions are outside the cell). Two types of Angiotensin-converting enzyme exist, ACE1 and ACE2, although the most focus has been on ACE1 which has been attributed with receptor-mediated effects like vasoconstriction, inflammation and cell growth/proliferation. <ref name="Ferrario">PMID:17083068</ref> The Renin-Angiotensin System (RAS) is a major regulator of blood pressure in the human body. [[Renin]] is an enzyme produced by the liver which cleaves Angiotensinogen into Angiotensin I Angiotensin Ihas the sequence, DRVTIHPFHL, and does not appear to have any biological activity. Angiotensin 1 (See:[[1n9u]]) is converted into Angiotensin II (See:[[1n9v]]) via the removal of the two C-terminal residues by ACE, yielding the active peptide: DRVTIHPF. <ref>PMID:12752436</ref>
-Angiotensin II interacts with two receptor subtypes, AT1 and AT2, which are widely distributed throughout the body. <ref name="Brew">PMID:12915047</ref> Binding of Angiotensin II to ATI leads to vasoconstriction by vascular smooth muscle cells, resulting in increased blood pressure, as well as the release of fluid and electrolyte homeostasis regulator, aldosterone, by the adrenal glands. Further, Angiotensin II binds to kidney AT1 receptors resulting in sodium ion reabsorption, leading to increased water retention in the blood and subsequent increased blood pressure. <ref name="Sturrock">PMID:15549168</ref> {| class="wikitable" border="1" width="60%" style="text-align:center" align=right
+Angiotensin II interacts with two receptor subtypes, AT1 and AT2, which are widely distributed throughout the body. <ref name="Brew">PMID:12915047</ref> Binding of Angiotensin II to ATI leads to vasoconstriction by vascular smooth muscle cells, resulting in increased blood pressure, as well as the release of fluid and electrolyte homeostasis regulator, aldosterone, by the adrenal glands. Further, Angiotensin II binds to kidney AT1 receptors resulting in sodium ion reabsorption, leading to increased water retention in the blood and subsequent increased blood pressure. <ref name="Sturrock">PMID:15549168</ref>
+{| class="wikitable" border="1" width="60%" style="text-align:center" align=right
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 !  colspan="2" align="center"| Selected AT1 and AT2 Receptor-Mediated Effects of Angiotensin II. <ref name="Weir"/><ref name="Ferrario"/>
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 |  Cardiovascular effects: Increased Atherogenicity, increased arrhythmogenicity, decreased renal blood flow, increased myocardial contractility.
 |  Cardiovascular Effects: Improved cardiac function and decreased chornotropic effect.
-|}Additionally, Bradykinin, which is inactivated by ACE1, has vasodilatory and cardioprotective properties by promoting the formation of nitric oxide by the [http://en.wikipedia.org/wiki/Endothelium endothelium]. <ref>PMID:12767053</ref> The essential role ACE1 plays in blood pressure homeostasis is further supported by knockout mice created by Cole et. al. ACE1 knockout mice exhibited an approximate 35% reduction in blood pressure, resulting in hypotension and subsequent organ damage. Thus despite the many systems contributing to blood pressure in mammals, i.e. nitric oxide, endothelin and andregenic stimulation etc. these redundant systems are not enough to overcome a disruption of the RAAS. <ref>PMID:11967804</ref> It should be noted that AT2 binding of Angiotensin II results in many processes that counterbalance the binding of AT1. See the schematic image of the Renin-Angiotensin-Aldosterone System at the left for a visual description and the table below for selected Angiotensin receptor-mediated effects of binding Angiotensin II.
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+Additionally, Bradykinin, which is inactivated by ACE1, has vasodilatory and cardioprotective properties by promoting the formation of nitric oxide by the [http://en.wikipedia.org/wiki/Endothelium endothelium]. <ref>PMID:12767053</ref> The essential role ACE1 plays in blood pressure homeostasis is further supported by knockout mice created by Cole et. al. ACE1 knockout mice exhibited an approximate 35% reduction in blood pressure, resulting in hypotension and subsequent organ damage. Thus despite the many systems contributing to blood pressure in mammals, i.e. nitric oxide, endothelin and andregenic stimulation etc. these redundant systems are not enough to overcome a disruption of the RAAS. <ref>PMID:11967804</ref> It should be noted that AT2 binding of Angiotensin II results in many processes that counterbalance the binding of AT1. See the schematic image of the Renin-Angiotensin-Aldosterone System at the left for a visual description and the table below for selected Angiotensin receptor-mediated effects of binding Angiotensin II.
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