Angiotensin's Role in Hypoxic Injury

In order to determine the mechanism in which the AT2 receptor protected cortical neuronal cultures from sodium azide-induced apoptosis. We show that K+ channels are required for AT2 receptor neuroprotection and more specifically the actions of the delayed rectifier K+ channel. We suggest that the yielding ionic effect resulting from the activation of the delayed rectifier K+ channel, was a transiently ionic preconditioned neuron, which could temporarily withstand the ionic stress, generated during hypoxia. We confirmed this theory by showing that the neuroprotective actions of the AT2 receptor are lost when the Na+/Ca+2 exchanger or the Na+/K + ATPase were blocked. In summary, our findings suggest that angiotensin's protective effect against chemical hypoxia results, at least in part, from ionic pre-conditioning and appears to be coupled to activation of the delayed rectifier K+ channel. However the Na+/Ca +2 exchanger and the Na+/K+ ATPase may also be directly modulated by angiotensin. Further understanding the role of ionic regulation during and after ischemia, and the potential actions of angiotensin, should provide insights into new therapeutic strategies for the treatment and/or the prevention of stroke injury.

Name thesis:degree_name

Ph.D.

Level thesis:degree_level

Dissertation

Discipline thesis:degree_discipline

Microbiology

Grantor

University of Illinois at Urbana-Champaign

Year dc:date

2015

Author dc:creator

• Grammatopoulos, Tom N.

Contributors dc:contributor

• Weyhenmeyer, James A.

• Biology, Neuroscience

Language dc:language

eng

Identifier

(MiAaPQ)AAI3070312

OAI identifier oai:identifier

oai:www.ideals.illinois.edu:2142/86643