Preclinical and clinical evaluation of autonomic function in humans

• Published in: The Journal of physiology 2016-07, Vol.594 (14), p.4009-4013
• Main Author: Joyner, Michael J.
• Format: Article
• Language: English
• Subjects: Autonomic Nervous System; Autonomic Nervous System - physiology; Blood pressure; Cardiovascular Physiology; Catecholamines - blood; Catecholamines - physiology; Heart Rate - physiology; Humans; Mortality; Special section reviews: Cardiac autonomic control in health and disease; Symposium Review
• ISSN: 0022-3751; 1469-7793
• DOI: 10.1113/JP271875

This review focuses on how to assess autonomic function in humans including various ways to measure heart rate, catecholamines, and sympathetic neural activity. The need to assess autonomic function is paramount in many experimental paradigms because of the following. (1) Autonomic dysfunction is present in common diseases like hypertension, diabetes and heart failure, and the magnitude of this dysfunction is broadly related to morbidity and mortality in these disorders. (2) The relationship between autonomic dysfunction and morbidity and mortality can be causal. (3) Interventions that modulate or reverse autonomic dysfunction can improve outcomes in the affected patients. The techniques discussed are also frequently used to understand the autonomic response to sympathoexcitatory manoeuvres like exercise, the cold pressor test or mental stress. Because these manoeuvres can engage a variety of sensory and efferent pathways, under some circumstances the physiological responses measured by many of the techniques are directionally similar, in others they are divergent. Thus any investigator seeking to study the autonomic nervous system or its contribution to either normal physiology or pathophysiological conditions must carefully balance a number of considerations to ensure that the right technique is used to address the question of interest. Schematic diagram highlighting how autonomic function can be measured in humans. (1) Heart rate can be measured and heart rate variability calculated to assess vagal tone. Blockade of ACH receptors with atropine eliminates heart rate variability. Blockade of noradrenaline (NA) with β‐adrenergic antagonists has little effect on heart rate variability; hence it is largely seen as an index of vagal tone. (2) Plasma NA concentrations and spillover can also be measured to assess sympathetic activity. (3) Peripheral sympathetic activity to skin and muscle can be measured directly with microneurography. (4) Manoeuvres that influence baroreceptor discharge can be used to evoke changes in heart rate and peripheral sympathetic activity to understand the dynamic components of key autonomic responses. Depending on issues related to experimental design, these techniques can be used to assess responses to various sympathoexcitatory stressors, and gain insight into physiological regulation.