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dc.contributor.authorChapman, Sandy.en_US
dc.date.accessioned2009-06-15T17:00:37Z
dc.date.available2009-06-15T17:00:37Z
dc.date.issued2008-06-15T17:00:37Z
dc.identifier.urihttp://hdl.handle.net/10464/1606
dc.description.abstractWith the relationship between endothelin-1 (ET-1) stimulation and reactive oxygen species (ROS) production unknown in adventitial fibroblasts, I examined the ROS response to ET-1 and angiotensin (Ang II). ET-1 -induced ROS peaked following 4 hrs of ET-1 stimulation and was inhibited by an ETA receptor antagonist (BQ 123, 1 uM) an extracellular signal-regulated kinase (ERK) 1/2 inhibitor (PD98059, 10 uM), and by both a specific, apocynin (10 uM), and non-specific, diphenyleneiodonium (10 uM), NAD(P)H oxidase inhibitor. NOX2 knockout fibroblasts did not produce an ET-1 induced change in ROS levels. Ang II treatment increased ROS levels in a biphasic manner, with the second peak occurring 6 hrs following stimulation. The secondary phase of Ang II induced ROS was inhibited by an ATi receptor antagonist, Losartan (100 uM) and BQ 123. In conclusion, ET-1 induces ROS production primarily through an ETA-ERKl/2 NOX2 pathway, additionally, Ang II-induced ROS production also involves an ETa pathway.en_US
dc.language.isoengen_US
dc.publisherBrock Universityen_US
dc.subjectEndothelinsen_US
dc.subjectCardiovascular agents.en_US
dc.subjectActive oxygenen_US
dc.subjectAngiotensin IIen_US
dc.titleMechanisms of endothelin-1 induced reactive oxygen species production in vascular adventitial fibroblastsen_US
dc.typeElectronic Thesis or Dissertationen_US
dc.degree.nameM.Sc. Applied Health Sciencesen_US
dc.degree.levelMastersen_US
dc.contributor.departmentApplied Health Sciences Programen_US


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