Lack of concordance between estimates of sympathetic transduction in humans

Abstract

The transduction of sympathetic nervous outflow into arterial vasoconstriction is critical for blood pressure homeostasis. Hence, there is an emerging field of sympathetic transduction to study human health and disease. Much of this work examines sympathetic transduction in response to spontaneous bursts of sympathetic activity. For these analyses, the dependent variable can be beat-by-beat changes in either systemic pressure (‘neurohemodynamic)’ or regional vascular conductance (‘neurovascular’). However, few studies have explored the concordance between changes in these two relations within individuals. Hypoxia induces increased sympathetic activity that is not accompanied by increased blood pressure; therefore, sympathetic transduction would seem to be altered. We assessed both ‘neurohemodynamic’ and ‘neurovascular’ sympathetic transduction during normoxia and sustained hypoxia (~80% SpO2) in young healthy individuals (N=7). Because hypoxia also induces tachycardia and tachypnea, we also assessed transduction(s) as a function of time rather than beat and after filtering out respiratory effects. Hypoxia induced significant (p<0.10) changes in heart rate (60+/-2 vs. 78+/-4 beats/min), respiration (5.8+/-0.3 vs. 8.7+/-1.2 L/min), and sympathetic activity (1431+/-256 vs.2066+/-470 aiu/min), but not in diastolic blood pressure (73+/-2 vs. 76+/-2 mmHg) or leg blood flow (11+/-1 vs. 11+/-1 cm/sec). This resulted in greater ‘neurohemodynamic’ (p<0.01) but no change in ‘neurovascular’ (p=0.94) sympathetic transduction. However, transduction(s) assessed as a function of time and after respiratory filtering demonstrated no effect on ‘neurohemodynamic’ (p=0.24) with a reduced ‘neurovascular’ (p=0.10) sympathetic transduction. These findings indicate that beat-by-beat systemic and regional estimates for transduction from spontaneous bursts of sympathetic activity may not reflect the linear relationship between sympathetic nervous outflow transduced into arterial vasoconstriction for blood pressure homeostasis. In addition, physiologic confounders, such as changes or differences in chronotropic and/or ventilatory state can exert profound influences on the estimated sympathetic transduction(s) and so should be considered if these analyses are to be pursued. This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.