Journal
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM
Volume 38, Issue 11, Pages 1993-2005Publisher
SAGE PUBLICATIONS INC
DOI: 10.1177/0271678X17724930
Keywords
Alzheimer disease; amyloid-beta peptides; baroreflex; Dahl salt-sensitive rats; hypertension
Categories
Funding
- Alzheimers Research UK [ART-PG2011-1, ARUK-PG2015-11] Funding Source: researchfish
- British Heart Foundation [RG/12/6/29670, PG/10/47/28285] Funding Source: researchfish
- British Heart Foundation [PG/10/47/28285, RG/12/6/29670] Funding Source: Medline
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Mid-life hypertension and cerebral hypoperfusion may be preclinical abnormalities in people who later develop Alzheimer's disease. Although accumulation of amyloid-beta (A beta) is characteristic of Alzheimer's disease and is associated with upregulation of the vasoconstrictor peptide endothelin-1 within the brain, it is unclear how this affects systemic arterial pressure. We have investigated whether infusion of A beta(40) into ventricular cerebrospinal fluid modulates blood pressure in the Dahl salt-sensitive rat. The Dahl salt-sensitive rat develops hypertension if given a high-salt diet. Intracerebroventricular infusion of A beta induced a progressive rise in blood pressure in rats with pre-existing hypertension produced by a high-salt diet (p < 0.0001), but no change in blood pressure in normotensive rats. The elevation in arterial pressure in high-salt rats was associated with an increase in low frequency spectral density in systolic blood pressure, suggesting autonomic imbalance, and reduced cardiac baroreflex gain. Our results demonstrate the potential for intracerebral A beta to exacerbate hypertension, through modulation of autonomic activity. Present findings raise the possibility that mid-life hypertension in people who subsequently develop Alzheimer's disease may in some cases be a physiological response to reduced cerebral perfusion complicating the accumulation of A beta within the brain.
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