2.50
Hdl Handle:
http://hdl.handle.net/10755/160189
Type:
Presentation
Title:
Fetal Origins of Hypertension: Placental Insufficiency Linking Cause and Effect
Abstract:
Fetal Origins of Hypertension: Placental Insufficiency Linking Cause and Effect
Conference Sponsor:Midwest Nursing Research Society
Conference Year:2007
Author:Anderson, Cindy, PhD
P.I. Institution Name:University of North Dakota
Contact Address:College of Nursing - Stop 9025, 430 Oxford Street, Room 307, Grand Forks, ND, 58202, USA
Co-Authors:F. Lopez and A. Zimmer, College of Nursing, University of North Dakota, Grand Forks, ND; and J.N. Benoit, Pharmacology, Physiology and Therapeutics, University of North Dakota, Grand Forks, ND
Placental insufficiency due to impaired vascular remodeling has been implicated as the cause of preeclampsia, initiating a sequence of events leading to onset hypertension in both mothers and their children. Barker's fetal origins of disease hypothesis proposes that cardiovascular disease results from developmental plasticity, or altered phenotype in response to adverse environmental conditions, induced by fetal undernutrition. Determining the underlying cause of this syndrome has been limited due to the invasive nature required of such studies in humans, requiring an animal model to study physiologic mechanisms mimicking the human condition, preeclampsia. The hypothesis tested in this study states that fetal exposure to placental insufficiency leads to the development and perpetuation of hypertension in two generations of offspring. Sprague-Dawley female rats were bred, with experimental pregnant (EP) rats undergoing a surgical procedure inducing placental insufficiency. Offspring born to control pregnant (CP) and EP rats comprise the first generation (F1) groups. F1 offspring comprise the second generation experimental group (F2). Biweekly weights and systolic blood pressures (SBP) were obtained from CP and EP groups prior to and during pregnancy. Weekly weights and SBP were measured in C, F1 and F2 offspring groups. Analyses included descriptive statistics, student's t test and ANOVA with Tukey contrasts. Significant increases in SBP in EP rats were induced by RUPP. SBP was significantly increased in experimental F1 offspring as early as 4 weeks of age. SBP increases were evident in F2 offspring by 5 weeks (juvenile period) in males, and by 9 weeks (adolescence) in females. These studies conclude that placental insufficiency stimulates hypertension in affected pregnant rats and their offspring. In addition, perpetuation of hypertension in a subsequent generation of offspring was precipitated by parental exposure to placental insufficiency during fetal development, suggesting the existence of the epigenetic transmission of cardiovascular alterations. These findings allow identification of high risk populations prior to the onset of clinical manifestations of hypertension, and potential for risk reduction through primary prevention strategies.
Repository Posting Date:
26-Oct-2011
Date of Publication:
17-Oct-2011
Sponsors:
Midwest Nursing Research Society

Full metadata record

DC FieldValue Language
dc.typePresentationen_GB
dc.titleFetal Origins of Hypertension: Placental Insufficiency Linking Cause and Effecten_GB
dc.identifier.urihttp://hdl.handle.net/10755/160189-
dc.description.abstract<table><tr><td colspan="2" class="item-title">Fetal Origins of Hypertension: Placental Insufficiency Linking Cause and Effect</td></tr><tr class="item-sponsor"><td class="label">Conference Sponsor:</td><td class="value">Midwest Nursing Research Society</td></tr><tr class="item-year"><td class="label">Conference Year:</td><td class="value">2007</td></tr><tr class="item-author"><td class="label">Author:</td><td class="value">Anderson, Cindy, PhD</td></tr><tr class="item-institute"><td class="label">P.I. Institution Name:</td><td class="value">University of North Dakota</td></tr><tr class="item-address"><td class="label">Contact Address:</td><td class="value">College of Nursing - Stop 9025, 430 Oxford Street, Room 307, Grand Forks, ND, 58202, USA</td></tr><tr class="item-email"><td class="label">Email:</td><td class="value">cindyanderson@mail.und.edu</td></tr><tr class="item-co-authors"><td class="label">Co-Authors:</td><td class="value">F. Lopez and A. Zimmer, College of Nursing, University of North Dakota, Grand Forks, ND; and J.N. Benoit, Pharmacology, Physiology and Therapeutics, University of North Dakota, Grand Forks, ND</td></tr><tr><td colspan="2" class="item-abstract">Placental insufficiency due to impaired vascular remodeling has been implicated as the cause of preeclampsia, initiating a sequence of events leading to onset hypertension in both mothers and their children. Barker's fetal origins of disease hypothesis proposes that cardiovascular disease results from developmental plasticity, or altered phenotype in response to adverse environmental conditions, induced by fetal undernutrition. Determining the underlying cause of this syndrome has been limited due to the invasive nature required of such studies in humans, requiring an animal model to study physiologic mechanisms mimicking the human condition, preeclampsia. The hypothesis tested in this study states that fetal exposure to placental insufficiency leads to the development and perpetuation of hypertension in two generations of offspring. Sprague-Dawley female rats were bred, with experimental pregnant (EP) rats undergoing a surgical procedure inducing placental insufficiency. Offspring born to control pregnant (CP) and EP rats comprise the first generation (F1) groups. F1 offspring comprise the second generation experimental group (F2). Biweekly weights and systolic blood pressures (SBP) were obtained from CP and EP groups prior to and during pregnancy. Weekly weights and SBP were measured in C, F1 and F2 offspring groups. Analyses included descriptive statistics, student's t test and ANOVA with Tukey contrasts. Significant increases in SBP in EP rats were induced by RUPP. SBP was significantly increased in experimental F1 offspring as early as 4 weeks of age. SBP increases were evident in F2 offspring by 5 weeks (juvenile period) in males, and by 9 weeks (adolescence) in females. These studies conclude that placental insufficiency stimulates hypertension in affected pregnant rats and their offspring. In addition, perpetuation of hypertension in a subsequent generation of offspring was precipitated by parental exposure to placental insufficiency during fetal development, suggesting the existence of the epigenetic transmission of cardiovascular alterations. These findings allow identification of high risk populations prior to the onset of clinical manifestations of hypertension, and potential for risk reduction through primary prevention strategies.</td></tr></table>en_GB
dc.date.available2011-10-26T22:42:34Z-
dc.date.issued2011-10-17en_GB
dc.date.accessioned2011-10-26T22:42:34Z-
dc.description.sponsorshipMidwest Nursing Research Societyen_GB
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