Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/61020
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Type: Journal article
Title: Angiotensin-converting enzyme (ACE) inhibitors exacerbate histological damage and motor deficits after experimental traumatic brain injury
Author: Harford-Wright, E.
Thornton, E.
Vink, R.
Citation: Neuroscience Letters, 2010; 481(1):26-29
Publisher: Elsevier Sci Ireland Ltd
Issue Date: 2010
ISSN: 0304-3940
1872-7972
Statement of
Responsibility: 
Elizabeth Harford-Wright, Emma Thornton and Robert Vink
Abstract: Angiotensin-converting enzyme (ACE) inhibitors are widely used as blood pressure medications in hypertensive individuals. However, ACE inhibitors also play an integral role in the breakdown of neuronal substance P, which has been recently implicated in the development of functional deficits following traumatic brain injury (TBI). The present study therefore examined the effects of ACE inhibitors on histological and motor outcome following TBI. Male Sprague-Dawley rats were treated with Captopril, Enalapril or equal volume saline for 7 days prior to the induction of diffuse TBI using the impact acceleration model. At 5h post-injury, animals administered Captopril demonstrated significantly increased substance P immunoreactivity compared to vehicle controls (p<0.01), and increased dark cell change that persisted to 7 days post-trauma. Captopril also resulted in exacerbated motor deficits compared to vehicle treated animals (p<0.05) as assessed by the rotarod test over a 7-day post-traumatic period. Administration of the alternative ACE inhibitor, Enalapril, likewise exacerbated motor deficits, confirming a class effect of ACE inhibitors rather than a compound effect specific to Captopril. We conclude that ACE inhibitors are deleterious to outcome following TBI, presumably by impairing the degradation of substance P and increasing substance P mediated neuronal injury.
Keywords: Captopril; Angiotensin-converting enzyme; Neurogenic inflammation; Substance P; Neurotrauma
Rights: Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.
RMID: 0020100383
DOI: 10.1016/j.neulet.2010.06.044
Appears in Collections:Pathology publications

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