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Crossing the intersection of human hypertension and adrenergic vasoconstriction using innovative methods

Journal of Human Hypertension volume 36, pages 1–2 (2022)Cite this article

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In the present issue of the Journal of Human Hypertension, Kobetic et al. [1] investigated the influence of human hypertension on transduction of muscle sympathetic nerve activity (MSNA) to arterial pressure (BP) (i.e., sympathetic transduction). The findings of this study were novel and of clinical importance because of the methodology that was employed and the target patient population. Previous studies examining α-adrenergic receptor sensitivity in human hypertension have included only intra-arterial infusion of agonists or antagonists in the forearm [2]. However, systemic BP responsiveness to MSNA cannot be fully extrapolated from studies examining α-adrenergic sensitivity only in the forearm circulation because vascular responsiveness to sympathetic innervation is heterogenous across vascular regions. For instance, the lower limbs exhibit greater vascular sensitivity to sympathetic stimulation compared with the forearm vasculature as a result of greater α-adrenergic receptor density and/or sensitivity in the lower limbs [3, 4]. Studies examining potential alterations in systemic BP responsiveness to MSNA in hypertensive patients have been lacking.

Sympathetic transduction is a technique that quantifies the systemic pressor response to spontaneous bursts of MSNA with high temporal resolution and has been performed extensively by only a few laboratories. The technique involves recording multiunit postganglionic MSNA with a tungsten microelectrode and bursts of MSNA act as a trigger and the ensuing BP signal is tracked for 15 subsequent cardiac cycles using signal averaging [5,6,7,8,9]. In contrast to previous studies, Kobetic et al. [1] employed an analysis that traveled backward in time (6–8 cardiac cycles) from a peak rise in BP to detect the occurrence of MSNA and the slope of the linear regression between the corresponding BP and MSNA values was determine. Although a direct comparison has not been made between these different approaches for analysis of sympathetic transduction, the fidelity of the technique employed by Kobetic et al. [1] provided the ability to detect a significantly lower slope of the linear regression among men with hypertension compared with men without hypertension. These findings set the stage for further analyses that more fully characterize sympathetic transduction by quantifying the impact of differing MSNA firing patterns on the BP response. For example, signal averaging is used to determine BP responses to multiple successive bursts of MSNA, which of course would promote larger pressor responses compared with only single bursts of MSNA [5,6,7,8,9]. Additionally, the contribution of MSNA burst amplitude to the ensuing MAP response can be determined.

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  1. Department of Anesthesiology, University of Kansas Medical Center, Kansas City, KS, USA

    Seth W. Holwerda

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Correspondence to Seth W. Holwerda.

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Holwerda, S.W. Crossing the intersection of human hypertension and adrenergic vasoconstriction using innovative methods. J Hum Hypertens 36, 1–2 (2022). https://doi.org/10.1038/s41371-021-00571-y

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