Vascular dysfunction in pulmonary hypertension: Role of protein kinase G-1a nitration

Hdl Handle:
http://hdl.handle.net/10675.2/344017
Title:
Vascular dysfunction in pulmonary hypertension: Role of protein kinase G-1a nitration
Authors:
Aggarwal, Saurbh
Abstract:
Pulmonary 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.
Affiliation:
Vascular Biology Center
Issue Date:
Jun-2011
URI:
http://hdl.handle.net/10675.2/344017
Additional Links:
http://ezproxy.gru.edu/login?url=http://search.proquest.com/docview/889027379?accountid=12365
Type:
Dissertation
Appears in Collections:
Theses and Dissertations

Full metadata record

DC FieldValue Language
dc.contributor.authorAggarwal, Saurbhen
dc.date.accessioned2015-01-30T19:14:59Z-
dc.date.available2015-01-30T19:14:59Z-
dc.date.issued2011-06-
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.en
dc.relation.urlhttp://ezproxy.gru.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.committeeFulton, David; Verin, Alexander; Lucas, Rudolf; Fineman, Jeffrey R.en
dc.description.degreeDoctor of Philosophy (Ph.D.)en
All Items in Scholarly Commons are protected by copyright, with all rights reserved, unless otherwise indicated.