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Role of angiotensin II type 1 receptor in cerebral aneurysm formation in rats

Tomohiro Aoki1, Masaki Nishimura, Hiroharu Kataoka

  • 1Department of Neurosurgery, Kyoto University, Graduate School of Medicine, Kyoto 606-8507, Japan.

International Journal of Molecular Medicine
|July 30, 2009
PubMed

Insights

Cerebral aneurysms (CAs) lack medical treatments. The renin-angiotensin system (RAS) does not appear to significantly contribute to CA formation, suggesting different mechanisms than other vascular diseases.

Area of Science:

  • Vascular Biology
  • Neuroscience
  • Pathophysiology

Background:

  • Cerebral aneurysms (CAs) lead to subarachnoid hemorrhage with high mortality.
  • Currently, no medical treatments exist for unruptured CAs, necessitating research into their formation.
  • Chronic inflammation at cerebral arterial bifurcations, driven by hemodynamic stress, contributes to CA development.

Purpose of the Study:

  • To investigate the role of the renin-angiotensin system (RAS) in cerebral aneurysm (CA) formation.
  • To determine if angiotensin (Ang) II type 1 receptor blockade affects CA development and inflammation.

Main Methods:

  • Analysis of Ang II type 1 receptor expression in cerebral aneurysmal walls.
  • Administration of Ang II type 1 receptor blockers in rat models of CA formation.
  • Assessment of inflammation in cerebral aneurysmal walls.

Main Results:

  • Angiotensin (Ang) II type 1 receptor was not upregulated in cerebral aneurysmal walls.
  • Subcutaneous administration of an Ang II type 1 receptor blocker did not inhibit CA formation or inflammation in rat models.
  • The renin-angiotensin system (RAS) appears to play a minor role in cerebral aneurysm formation.

Conclusions:

  • The renin-angiotensin system (RAS) may not be a primary driver in cerebral aneurysm (CA) pathogenesis.
  • Mechanisms underlying cerebral aneurysm formation may differ significantly from those of aortic aneurysms and other vascular diseases.

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