Dysfunctional Control of Coronary Blood Flow in Renovascular Hypertension

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dc.contributor.advisorGwirtz, Patricia A.
dc.contributor.committeeMemberShi, Xiangrong
dc.contributor.committeeMemberRaven, Peter B.
dc.creatorKline, Geoffrey Philip
dc.date.accessioned2019-08-22T20:39:06Z
dc.date.available2019-08-22T20:39:06Z
dc.date.issued1999-06-01
dc.date.submitted2013-09-13T08:54:07-07:00
dc.description.abstractKline, Geoffrey Philip, Dysfunctional Control of Coronary Blood Flow in Renovascular Hypertension Doctor of Philosophy (Biomedical Sciences), June 1999, 98 pp, 2 tables, 10 figures, references, 142 titles. This study was designed to determine the effects of renovascular hypertension (RVH) on coronary vasoreactivity in conscious, chronically instrumented dogs. Six dogs were instrumented to measure left ventricular pressure, +dP/dtmax, heart rate, mean aortic pressure, circumflex blood flow (CBF), and cardiac output. In order to examine endothelial-dependent and independent coronary vasodilation, intracoronary injections of actylcholine (Ach), bradykinin (BDK), and sodium nitroprusside (SNP) were studied before and after induction of RVH in the presence and absence of nitric oxide (NO) blockade. After RVH, resting CBF was significantly reduced (P [less than] 0.05). In the normotensive state, NO-blockade significantly reduced the coronary vasodilation to Ach and BDK (P [less than] 0.05), but not SNP. After RVH, the coronary vasodilation to Ach, BDK, and SNP were reduced (P[less than] 0.05). After RVH, NO-blockade further reduced the coronary vasodilation to BDK (P [less than] 0.05), but not Ach. Thus, RVH resulted in an impairment of both endothelial-dependent and –independent coronary vasodilation. It also appears that during RVH the endothelium retains the ability to produce/release NO to some, but not all, stimuli. In order to examine the possibility that β-adrenergic mediated coronary vasodilation is impaired after RVH, intracoronary injections of norepinephrine (NE), isoproterenol (ISO), and terbutaline (TRB) were administered. These drugs all caused dose dependent increases in CBF before and after RVH. After RVH, the coronary vasodilatory responses to NE, ISO and TRB were significantly reduced (P [less than] 0.05). β1-blockade with intracoronary atenolol (1 mg) reduced the ISO-induced increases in CBF and had no effect on TRB responses (P [less than] 0.05). β2-blockade with intracoronary ICI-118,551 (1 mg) reduced the ISO-induced coronary vasodilation and abolished TRB responses (p[less than] 0.05). During β2-blockade, ISO-induced increases in CBF were not different after RVH. Therefore, these data indicate that β1-adrenergic mediated coronary vasodilation is preserved after RVH, whereas, β2-mediated is not. We conclude that 1) RVH results in an impairment of both endothelial-dependent and –independent coronary vasodilation; 2) RVH results in an impairment of β2-adrenergic mediated coronary vasodilation.
dc.format.mimetypeapplication/pdf
dc.identifier.urihttps://hdl.handle.net/20.500.12503/28624
dc.language.isoen
dc.provenance.legacyDownloads0
dc.subjectAnimal Sciences
dc.subjectCardiology
dc.subjectCardiovascular Diseases
dc.subjectCardiovascular System
dc.subjectKinesiology
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.subjectMotor Control
dc.subjectSmall or Companion Animal Medicine
dc.subjectVeterinary Medicine
dc.subjectDysfunctional control
dc.subjectcoronary blood flow
dc.subjectrenovascular hypertension
dc.subjectdogs
dc.subjectnitric oxide blockade
dc.subjectcoronary vasodilation
dc.titleDysfunctional Control of Coronary Blood Flow in Renovascular Hypertension
dc.typeDissertation
dc.type.materialtext
thesis.degree.departmentGraduate School of Biomedical Sciences
thesis.degree.disciplineBiomedical Sciences
thesis.degree.grantorUniversity of North Texas Health Science Center at Fort Worth
thesis.degree.nameDoctor of Philosophy

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