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dc.contributor.advisorRestifo, Linda L.en
dc.contributor.authorSalamanca, Melissa
dc.creatorSalamanca, Melissaen
dc.date.accessioned2016-11-30T20:50:58Z
dc.date.available2016-11-30T20:50:58Z
dc.date.issued2016
dc.identifier.urihttp://hdl.handle.net/10150/621455
dc.description.abstractHeart Failure is the state in which the heart is unable to pump enough blood to meet the needs of the body, resulting from events that progressively damage the myocardium and/or its ability to contract normally. Several compensatory mechanisms allow for short-term maintenance of adequate delivery of blood to the body. Progression from the initial events to heart failure is caused by the accumulation of pathologic changes and their effects, many of which result from chronic activation of these compensatory mechanisms. One of these mechanisms is the activation of the neurohormonal β-adrenergic system, to which the β₃-adrenergic receptor (β₃-AR) belongs. Research on the role of the β₃-AR in the heart has focused on the short-term protective role of the receptor, based on its ability to reduce the effects of over-stimulation of the heart's other adrenergic-system components. However, during the course of heart failure, its up-regulation and functional persistence may also contribute to the progression of the disease. There have been few large-animal studies, no human trials, and no long-term studies of β₃-AR agonists for use in the treatment of heart failure. Ultimately, individualized treatment strategies that, over time, modulate the relative levels of agonistic and antagonistic effects across each of the three β₃-AR subtypes, may be most effective for management of heart failure. However, further research and trials with β₃-AR agonists are realistic and necessary places to start.
dc.language.isoen_USen
dc.publisherThe University of Arizona.en
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en
dc.subjectCellular and Molecular Medicineen
dc.titleBeta₃-adrenergic receptors in the heart: Normal functions and potential roles in heart failureen_US
dc.typetexten
dc.typeElectronic Thesisen
thesis.degree.grantorUniversity of Arizonaen
thesis.degree.levelmastersen
dc.contributor.committeememberRestifo, Linda L.en
dc.contributor.committeememberDoetschman, Thomas C.en
dc.contributor.committeememberElliott, David A.en
thesis.degree.disciplineGraduate Collegeen
thesis.degree.disciplineCellular and Molecular Medicineen
thesis.degree.nameM.S.en
refterms.dateFOA2018-09-11T15:54:53Z
html.description.abstractHeart Failure is the state in which the heart is unable to pump enough blood to meet the needs of the body, resulting from events that progressively damage the myocardium and/or its ability to contract normally. Several compensatory mechanisms allow for short-term maintenance of adequate delivery of blood to the body. Progression from the initial events to heart failure is caused by the accumulation of pathologic changes and their effects, many of which result from chronic activation of these compensatory mechanisms. One of these mechanisms is the activation of the neurohormonal β-adrenergic system, to which the β₃-adrenergic receptor (β₃-AR) belongs. Research on the role of the β₃-AR in the heart has focused on the short-term protective role of the receptor, based on its ability to reduce the effects of over-stimulation of the heart's other adrenergic-system components. However, during the course of heart failure, its up-regulation and functional persistence may also contribute to the progression of the disease. There have been few large-animal studies, no human trials, and no long-term studies of β₃-AR agonists for use in the treatment of heart failure. Ultimately, individualized treatment strategies that, over time, modulate the relative levels of agonistic and antagonistic effects across each of the three β₃-AR subtypes, may be most effective for management of heart failure. However, further research and trials with β₃-AR agonists are realistic and necessary places to start.


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