New Findings: What is the central question of this study? Standing up can cause hypotension and tachycardia. Accumulated evidence poses the simple question, does the cardiac baroreflex operate at the onset of standing up? If the cardiac baroreflex is suppressed, what mechanism is responsible for baroreflex inhibition? What is the main finding and its importance? In cats, we found blunting of cardiac baroreflex sensitivity in the pressor range at the onset of voluntary hindlimb standing, but not of passive hindlimb standing. This finding suggests that central command suppresses pressor-evoked bradycardia at the onset of standing up, probably in advance, to prevent or buffer orthostatic hypotension.
Abstract: It remains unclear whether cardiac baroreflex function is preserved or suppressed at the onset of standing up. To answer the question and, if cardiac baroreflex is suppressed, to investigate the mechanism responsible for the suppression, we compared the sensitivity of the arterial cardiac baroreflex at the onset of voluntary and passive hindlimb standing in conscious cats. Cardiac baroreflex sensitivity was estimated from the maximal slope of the baroreflex curve between the responses of systolic arterial blood pressure and heart rate to a brief occlusion of the abdominal aorta. The systolic arterial blood pressure response to standing up without aortic occlusion was greater in the voluntary case than in the passive case. Cardiac baroreflex sensitivity was clearly decreased at the onset of voluntary standing up compared with rest (P = 0.005) and the onset of passive standing up (P = 0.007). The cardiac baroreflex sensitivity at the onset of passive standing up was similar to that at rest (P = 0.909). The findings suggest that central command would transmit a modulatory signal to the cardiac baroreflex system during the voluntary initiation of standing up. Furthermore, the present data tempt speculation on a close relationship between central inhibition of the cardiac baroreflex and the centrally induced tachycardiac response to standing up.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10103771 | PMC |
http://dx.doi.org/10.1113/EP090718 | DOI Listing |
Eur J Prev Cardiol
January 2025
Amsterdam UMC, University of Amsterdam, Department Vascular Medicine, Amsterdam Cardiovascular Sciences, Amsterdam, The Netherlands.
Aims: Cross-correlation baroreflex sensitivity (xBRS) and heart rate variability (HRV) are measures of autonomic cardiac control and are associated with hypertension. However, their value in predicting new-onset hypertension and changes in systolic blood pressure (SBP) remains elusive.
Methods: We used longitudinal data of participants with- and without a history of cardiovascular disease from the HEalthy Life In an Urban Setting (HELIUS) study.
JACC Heart Fail
January 2025
The Zena and Michael A. Wiener Cardiovascular Institute, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
PM R
January 2025
Department of Physical Medicine and Rehabilitation, Mayo Clinic, Rochester, Minnesota, USA.
Background: Individuals with spinal cord injury (SCI) commonly have autonomic dysreflexia (AD) with increased sympathetic activity. After SCI, individuals have decreased baroreflex sensitivity and increased vascular responsiveness.
Objective: To evaluate the relationship between baroreflex and blood vessel sensitivity with AD symptoms.
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 PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!