Molecules 2010, 15(9), 6598-6618; doi:10.3390/molecules15096598
Review

Kinin Receptor Antagonists as Potential Neuroprotective Agents in Central Nervous System Injury

1 Discipline of Anatomy and Pathology, School of Medical Sciences, University of Adelaide, South Australia, Australia 2 Adelaide Centre for Neuroscience Research, University of Adelaide, South Australia, Australia
* Author to whom correspondence should be addressed.
Received: 16 August 2010; in revised form: 10 September 2010 / Accepted: 14 September 2010 / Published: 20 September 2010
(This article belongs to the Special Issue Neuroprotective Strategies)
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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: brain injury; neurotrauma; stroke; neuropeptides; kinins

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MDPI and ACS Style

Thornton, E.; Ziebell, J.M.; Leonard, A.V.; Vink, R. Kinin Receptor Antagonists as Potential Neuroprotective Agents in Central Nervous System Injury. Molecules 2010, 15, 6598-6618.

AMA Style

Thornton E, Ziebell JM, Leonard AV, Vink R. Kinin Receptor Antagonists as Potential Neuroprotective Agents in Central Nervous System Injury. Molecules. 2010; 15(9):6598-6618.

Chicago/Turabian Style

Thornton, Emma; Ziebell, Jenna M; Leonard, Anna V; Vink, Robert. 2010. "Kinin Receptor Antagonists as Potential Neuroprotective Agents in Central Nervous System Injury." Molecules 15, no. 9: 6598-6618.

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