Angiotensin II [Neurosurgery Wiki]

This page is read only. You can view the source, but not change it. Ask your administrator if you think this is wrong.

====== Angiotensin II ======

[[Angiotensin]] I is converted to angiotensin II (AII) through the removal of two C-terminal residues by the enzyme angiotensin-converting enzyme ([[ACE]]), primarily through ACE within the lung (but also present in endothelial cells, kidney epithelial cells, and the brain). Angiotensin II acts on the central nervous system to increase vasopressin production, and also acts on venous and arterial smooth muscle to cause vasoconstriction. Angiotensin II also increases aldosterone secretion; it, therefore, acts as an endocrine, autocrine/paracrine, and intracrine hormone.
----
[[Iron]] overload plays a key role in secondary bleeding after ICH in [[Angiotensin II]]-induced hypertensive mice. Iron chelation during the process of Ang II-induced hypertension suppresses secondary bleeding after ICH
((Wang J, Tang XQ, Xia M, Li CC, Guo C, Ge HF, Yin Y, Wang B, Chen WX, Feng H. Iron chelation suppresses secondary bleeding after intracerebral hemorrhage in angiotensin II-infused mice. CNS Neurosci Ther. 2021 Aug 4. doi: 10.1111/cns.13706. Epub ahead of print. PMID: 34346561.)).

===== Angiotensin II receptor =====

[[Angiotensin II receptor]]