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.
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http://dx.doi.org/10.1016/j.lfs.2004.03.018 | DOI Listing |
Acta Physiol (Oxf)
February 2025
Department of Physiology, Graduate School of Health and Sports Science, Juntendo University, Chiba, Japan.
Aim: Chronic stress elevates blood pressure, whereas regular exercise exerts antistress and antihypertensive effects. However, the mechanisms of stress-induced hypertension and preventive effects through exercise remain unknown. Thus, we investigated the molecular basis involved in autonomic blood pressure regulation within the amygdala.
View Article and Find Full Text PDFFront Neurol
December 2024
Center for Data Science, Nell Hodgson Woodruff School of Nursing, Emory University, Atlanta, GA, United States.
Background: Traumatic brain injury (TBI) disrupts normal brain tissue and functions, leading to high mortality and disability. Severe TBI (sTBI) causes prolonged cognitive, functional, and multi-organ dysfunction. Dysfunction of the autonomic nervous system (ANS) after sTBI can induce abnormalities in multiple organ systems, contributing to cardiovascular dysregulation and increased mortality.
View Article and Find Full Text PDFAm J Physiol Heart Circ Physiol
January 2025
Department of Pharmacology, Physiology and Neurobiology, University of Cincinnati College of Medicine, Cincinnati, OH.
Lower body negative pressure (LBNP) has been used for decades in humans to model arterial baroreceptor unloading and represents a powerful tool for evaluating cardiovascular responses to orthostatic challenge. However, LBNP studies in animals have been limited to conditions of anesthesia or sedation, where cardiovascular reflexes are altered. Given the consequent uncertainties, the usefulness of LBNP studies in these preclinical models has been severely hampered.
View Article and Find Full Text PDFJ Biol Rhythms
January 2025
Department of Physiology, College of Medicine, University of Kentucky, Lexington, Kentucky.
Cardiovascular health requires the orchestration of the daily rhythm of blood pressure (BP), which responds to changes in light exposure and dietary patterns. Whether rhythmic light and feeding can modulate daily BP rhythm directly or via modulating intrinsic core clock gene is unknown. Using inducible global knockout mice (iBmal1KO), we explored the impact of rhythmic light, rhythmic feeding, or their combination on various physiological parameters.
View Article and Find Full Text PDFPurpose: Pre-clinical studies have demonstrated direct influences of the autonomic nervous system (ANS) on the immune system. However, it remains unknown if connections between the peripheral ANS and immune system exist in humans and contribute to the development of chronic inflammatory disease. This study had three aims: 1.
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