Experimental hypertension increases spontaneous intracerebral hemorrhages in a mouse model of cerebral amyloidosis

J Cereb Blood Flow Metab. 2016 Feb;36(2):399-404. doi: 10.1177/0271678X15606720. Epub 2015 Oct 2.

Abstract

Hypertension and cerebral amyloid angiopathy (CAA) are major risk factors for intracerebral hemorrhage (ICH); however the mechanisms of interplay between the two are not fully understood. We investigated the effect of hypertension in a transgenic mouse model with Alzheimer's-like pathology (Tg2576) treating them with angiotensin II and L-N(G)-nitroarginine methyl ester. A similar increase in systolic blood pressure was observed in both Tg2576 and control mice; however Tg2576 mice developed signs of stroke with a markedly shorter latency. Cerebral deposition of amyloid beta promotes the hypertension-induced ICH, thus supporting the notion that hypertension is a risk factor for ICH among patients with CAA.

Keywords: Alzheimer’s disease; cerebral amyloid angiopathy; hypertension; intracerebral hemorrhage; risk factors.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alzheimer Disease / genetics
  • Alzheimer Disease / pathology
  • Amyloid beta-Peptides / metabolism
  • Angiotensin II / pharmacology
  • Animals
  • Blood Pressure / drug effects
  • Brain / pathology
  • Cerebral Amyloid Angiopathy / complications*
  • Cerebral Amyloid Angiopathy / pathology
  • Female
  • Humans
  • Hypertension / complications*
  • Hypertension / pathology
  • Intracranial Hemorrhage, Hypertensive / etiology*
  • Intracranial Hemorrhage, Hypertensive / pathology
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • NG-Nitroarginine Methyl Ester / pharmacology
  • Risk Factors
  • Stroke / etiology
  • Stroke / pathology

Substances

  • Amyloid beta-Peptides
  • Angiotensin II
  • NG-Nitroarginine Methyl Ester