Intravascular β-amyloid infusion increases blood pressure : implications for a vasoactive role of β-amyloid in the pathogenesis of Alzheimer's disease

• Published in: Neuroscience letters 1999-06, Vol.268 (1), p.17-20
• Main Authors: ARENDASH, G. W, SU, G. C, CRAWFORD, F. C, BJUGSTAD, K. B, MULLAN, M
• Format: Article
• Language: English
• Subjects: Alzheimer Disease - etiology; Alzheimer Disease - physiopathology; Amyloid beta-Peptides - pharmacology; Animals; Biological and medical sciences; Blood Pressure - drug effects; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases; Female; Infusions, Intra-Arterial; Medical sciences; Neurology; Rats; Rats, Sprague-Dawley; Vasoconstrictor Agents - pharmacology
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/S0304-3940(99)00239-6

Hypertension has been recognized as a risk factor for Alzheimer's disease (AD). Moreover, serum beta-amyloid (A beta) levels are elevated in several mutations linked to familial AD, as well as in some sporadic AD individuals. To determine the in vivo effects of A beta on blood pressure, A beta(1-40) was infused intra-arterially into anesthetized rats. For all animals, strong correlations exist between pre-infusion mean arterial blood pressure (MA beta) and post-arterial infusion increases in blood pressure. In spontaneously hypotensive animals, A beta infusion resulted in substantial increases in MA beta compared to vehicle distilled water infusion. A beta(1-40) was also able to accelerate MA beta return from induced hypotension, but infusion of A beta(1-42), or rat amylin had no such effect. These results provide evidence that circulating A beta(1-40) can exert vasopressor actions in vivo. Moreover, they suggest a pathophysiologic role for vascular A beta in AD that precedes A beta deposition and dementia onset.