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dc.contributor.authorAggarwal, Saurbh
dc.date.accessioned2015-01-30T19:14:59Z
dc.date.available2015-01-30T19:14:59Z
dc.date.issued2011-06en
dc.identifier.urihttp://hdl.handle.net/10675.2/344017
dc.description.abstractPulmonary hypertension is a common and debilitating complication of pulmonary, cardiac, and extrathoracic pathologies. The development of pulmonary hypertension is associated with elevated pulmonary arterial pressure (PAP), and increased vascular remodeling. Pulmonary vascular tone is regulated through the activation of protein kinase G-la (PKG-la), which is the isoform predominantly found in the lungs, via a complex signaling pathway that involves nitric oxide (NO), natriuretic peptides (NP), and cyclic guanosine monophosphate (cGMP). Vascular injury secondary to increased reactive oxygen (ROS) and nitrogen species (RNS) in pulmonary hypertension disrupts these regulatory mechanisms, potentiating the development of vascular dysfunction. However, the molecular mechanisms underlying this dysfunction are not completely understood and were the focus of this study.
dc.relation.urlhttp://ezproxy.augusta.edu/login?url=http://search.proquest.com/docview/889027379?accountid=12365en
dc.rightsCopyright protected. Unauthorized reproduction or use beyond the exceptions granted by the Fair Use clause of U.S. Copyright law may violate federal law.en
dc.subjectPulmonary hypertensionen
dc.titleVascular dysfunction in pulmonary hypertension: Role of protein kinase G-1a nitrationen
dc.typeDissertationen
dc.contributor.departmentVascular Biology Centeren
dc.description.advisorBlack, Stephen M.en
dc.description.degreeDoctor of Philosophy (Ph.D.)en
dc.description.committeeFulton, David; Verin, Alexander; Lucas, Rudolf; Fineman, Jeffrey R.en
html.description.abstractPulmonary hypertension is a common and debilitating complication of pulmonary, cardiac, and extrathoracic pathologies. The development of pulmonary hypertension is associated with elevated pulmonary arterial pressure (PAP), and increased vascular remodeling. Pulmonary vascular tone is regulated through the activation of protein kinase G-la (PKG-la), which is the isoform predominantly found in the lungs, via a complex signaling pathway that involves nitric oxide (NO), natriuretic peptides (NP), and cyclic guanosine monophosphate (cGMP). Vascular injury secondary to increased reactive oxygen (ROS) and nitrogen species (RNS) in pulmonary hypertension disrupts these regulatory mechanisms, potentiating the development of vascular dysfunction. However, the molecular mechanisms underlying this dysfunction are not completely understood and were the focus of this study.


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