Nitric oxide and cerebral ischemic preconditioning.
Nitric oxide (NO) is an important mediator of cerebral blood flow and metabolism. As a vasodilator, NO regulates cerebral blood flow, and couples regional brain perfusion with metabolic activity. Following cerebral ischemia, NO levels rise significantly due to activation of neuronal nitric oxide synthase by NMDA receptor mediated calcium entry. Depending on its tissue and enzymatic source, NO may be protective or toxic. This article reviews the effects of NO following cerebral ischemia, the signaling pathways through which NO acts, and its potential roles in cerebral ischemic preconditioning.
Huang
Paul L
PL
Harvard Medical School, Cardiology Division and Cardiovascular Research Center, Massachusetts General Hospital, 149 Thirteenth Street, Charlestown, MA 02129, USA. phuang1@partners.org
D000818:Animals; D002545:Brain Ischemia / Q000201:enzymology / Q000378:metabolism*; D006801:Humans; D019194:Ischemic Preconditioning / Q000379:methods*; D009569:Nitric Oxide / Q000502:physiology*; D019001:Nitric Oxide Synthase / Q000502:physiology; D052248:Nitric Oxide Synthase Type I
D009569:Nitric Oxide; C496320:NOS1 protein, human; D019001:Nitric Oxide Synthase; D052248:Nitric Oxide Synthase Type I