{Reference Type}: Journal Article
{Title}: Interaction of simultaneous hypoxia and baroreflex loading on control of sympathetic action potential subpopulations.
{Author}: Boyes NG;Klassen SA;Baker SE;Nicholson WT;Joyner MJ;Shoemaker JK;Limberg JK;
{Journal}: J Neurophysiol
{Volume}: 0
{Issue}: 0
{Year}: 2024 Aug 14
{Factor}: 2.974
{DOI}: 10.1152/jn.00277.2024
{Abstract}: Efferent muscle sympathetic nerve activity (MSNA) is under tonic baroreflex control. The arterial baroreflex exerts the strongest influence over medium-sized sympathetic action potential (AP) subpopulations in efferent MSNA recordings. Prior work from multi-unit MSNA recordings has shown baroreflex loading selectively abolishes the sympathetic response to hypoxia. The purpose of the study was to examine baroreflex control over different-sized AP clusters and characterize the neural recruitment strategies of sympathetic AP subpopulations with baroreflex and combined baroreflex/chemoreflex (i.e., hypoxia) activation. We loaded the arterial baroreceptors (intravenous phenylephrine) alone and in combination with systemic hypoxia (SpO2 80%) in 9 healthy young men. We extracted sympathetic APs using wavelet-based methodology and quantified baroreflex gain for individual AP clusters. AP baroreflex threshold gain was measured as the slope of the linear relationship between AP probability versus diastolic blood pressure for 10 normalized clusters. Baroreflex loading with phenylephrine decreased MSNA and AP firing compared to baseline (all P < 0.05). However, the phenylephrine-mediated decrease in AP firing was lost with concurrent hypoxia (P = 0.384). Compared with baseline, baroreflex loading reduced medium sized AP cluster baroreflex threshold slope (condition P = 0.005) and discharge probability (condition P < 0.0001); these reductions from baseline were maintained during simultaneous hypoxia (both P < 0.05). Present findings indicate a key modulatory role of the baroreceptors on medium-sized APs in blood pressure regulation that withstands competing signals from peripheral chemoreflex activation.