Kinin Receptor Antagonists as Potential Neuroprotective Agents in Central Nervous System Injury
Open Access
- 19 September 2010
- Vol. 15 (9), 6598-6618
- https://doi.org/10.3390/molecules15096598
Abstract
Injury to the central nervous system initiates complex physiological, cellular and molecular processes that can result in neuronal cell death. Of interest to this review is the activation of the kinin family of neuropeptides, in particular bradykinin and substance P. These neuropeptides are known to have a potent pro-inflammatory role and can initiate neurogenic inflammation resulting in vasodilation, plasma extravasation and the subsequent development of edema. As inflammation and edema play an integral role in the progressive secondary injury that causes neurological deficits, this review critically examines kinin receptor antagonists as a potential neuroprotective intervention for acute brain injury, and more specifically, traumatic brain and spinal cord injury and stroke.Keywords
This publication has 117 references indexed in Scilit:
- Inhibition of Bradykinin Receptor B1 Protects Mice from Focal Brain Injury by Reducing Blood–Brain Barrier Leakage and InflammationJournal of Cerebral Blood Flow & Metabolism, 2010
- Quantitative analysis of cellular inflammation after traumatic spinal cord injury: evidence for a multiphasic inflammatory response in the acute to chronic environmentBrain, 2010
- Differential regulation of inducible and endothelial nitric oxide synthase by kinin B1 and B2 receptorsNeuropeptides, 2010
- Response to: The BRAIN TRIAL: a randomised, placebo controlled trial of a Bradykinin B2 receptor antagonist (Anatibant) in patients with traumatic brain injuryTrials, 2009
- The BRAIN TRIAL: a randomised, placebo controlled trial of a Bradykinin B2 receptor antagonist (Anatibant) in patients with traumatic brain injuryTrials, 2009
- The Role of Bradykinin B1 and B2 Receptors for Secondary Brain Damage after Traumatic Brain Injury in MiceJournal of Cerebral Blood Flow & Metabolism, 2009
- Ischemic Postconditioning as a Novel Avenue to Protect against Brain Injury after StrokeJournal of Cerebral Blood Flow & Metabolism, 2009
- Blood–spinal cord barrier permeability in experimental spinal cord injury: dynamic contrast‐enhanced MRINMR in Biomedicine, 2008
- Neuroinflammation, oxidative stress, and the pathogenesis of Parkinson’s diseaseClinical Neuroscience Research, 2006
- Acute and chronic changes in aquaporin 4 expression after spinal cord injuryNeuroscience, 2006