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.
- Angiotensin II
- Corticotropin Releasing Hormone
- Paraventricular Nucleus