TY - JOUR
T1 - Effect of chronic stress on the cardiac baroreflex in the post-weanling rat
AU - Porter, James P.
AU - Phillips, Adam
AU - Rich, Jason
AU - Wright, Danielle
N1 - Funding Information:
The work was funded by a Grant-in-Aid from the Western States Affiliate of the American Heart Association. D. Wright was a summer research student supported by NSF REU Site DBI9912126. The losartan was generously provided by Merck, Inc. and Du Pont, Rahway, NJ.
PY - 2004/8/13
Y1 - 2004/8/13
N2 - There is increasing evidence that early life stressors may program blood pressure control mechanisms such that the risk for cardiovascular disease in later life is increased. In the present investigation, the effect of repeated restraint/heat stress during the two-week period immediately after weaning on baroreflex function was determined and the contribution of brain angiotensin II (ANG II) to the changes was assessed in young, conscious, freely moving Sprague Dawley rats. In rats two weeks post weaning, basal MAP was significantly higher and basal HR significantly lower than rats tested immediately after weaning. This change in the operating point of HR was not accompanied by any changes in baroreflex function. Treatment with chronic icv infusion of losartan, an AT1 receptor antagonist, during the two-week period prevented the changes in basal MAP and HR. Chronic stress during the two weeks post weaning, whether due to surgical implantation of icv cannulae or due to restraint/heat stress, significantly shifted the set-point of the baroreflex function to a higher pressure. Chronic icv infusion of losartan during the period prevented these effects (at least in the case of stress due to the presence of icv cannulae) suggesting a role for brain ANG II in the change. Changes in the expression of CRH mRNA in the paraventricular nucleus could not explain the stress-related change in baroreflex function. If the rightward shift in the baroreflex persists into adulthood, it could increase the susceptibility to cardiovascular diseases such as hypertension.
AB - There is increasing evidence that early life stressors may program blood pressure control mechanisms such that the risk for cardiovascular disease in later life is increased. In the present investigation, the effect of repeated restraint/heat stress during the two-week period immediately after weaning on baroreflex function was determined and the contribution of brain angiotensin II (ANG II) to the changes was assessed in young, conscious, freely moving Sprague Dawley rats. In rats two weeks post weaning, basal MAP was significantly higher and basal HR significantly lower than rats tested immediately after weaning. This change in the operating point of HR was not accompanied by any changes in baroreflex function. Treatment with chronic icv infusion of losartan, an AT1 receptor antagonist, during the two-week period prevented the changes in basal MAP and HR. Chronic stress during the two weeks post weaning, whether due to surgical implantation of icv cannulae or due to restraint/heat stress, significantly shifted the set-point of the baroreflex function to a higher pressure. Chronic icv infusion of losartan during the period prevented these effects (at least in the case of stress due to the presence of icv cannulae) suggesting a role for brain ANG II in the change. Changes in the expression of CRH mRNA in the paraventricular nucleus could not explain the stress-related change in baroreflex function. If the rightward shift in the baroreflex persists into adulthood, it could increase the susceptibility to cardiovascular diseases such as hypertension.
KW - Angiotensin II
KW - Baroreceptor
KW - Corticotropin Releasing Hormone
KW - Paraventricular Nucleus
UR - http://www.scopus.com/inward/record.url?scp=3142762312&partnerID=8YFLogxK
U2 - 10.1016/j.lfs.2004.03.018
DO - 10.1016/j.lfs.2004.03.018
M3 - Article
C2 - 15261764
AN - SCOPUS:3142762312
SN - 0024-3205
VL - 75
SP - 1595
EP - 1607
JO - Life Sciences
JF - Life Sciences
IS - 13
ER -