Abstract
Transduction of muscle sympathetic nerve activity (MSNA) into vascular tone varies with age and sex. Older normotensive men have reduced sympathetic transduction so that a given level of MSNA causes less arteriole vasoconstriction. Whether sympathetic transduction is altered in hypertension (HTN) is not known. We investigated whether sympathetic transduction is impaired in untreated hypertensive men compared to normotensive controls. Eight untreated hypertensive men and 10 normotensive men (age 50 ± 15 years vs. 45 ± 12 years (mean ± SD); p = 0.19, body mass index (BMI) 24.7 ± 2.7 kg/m2 vs. 26.0 ± 4.2 kg/m2; p = 0.21) were recruited. MSNA was recorded from the peroneal nerve using microneurography; beat-to-beat blood pressure (BP; Finapres) and heart rate (ECG) were recorded simultaneously at rest for 10 min. Sympathetic-transduction was quantified using a previously described method. The relationship between MSNA burst area and subsequent diastolic BP was measured for each participant with the slope of the regression indicating sympathetic transduction. MSNA was higher in the hypertensive group compared to normotensives (73 ± 17 bursts/100 heartbeats vs. 49 ± 19 bursts/100 heart bursts; p = 0.007). Sympathetic-transduction was lower in the hypertensive versus normotensive group (0.04%/mmHg/s vs. 0.11%/mmHg/s, respectively; R = 0.622; p = 0.006). In summary, hypertensive men had lower sympathetic transduction compared to normotensive individuals suggesting that higher levels of MSNA are needed to cause the same level of vasoconstrictor tone.
Highlights
The arrival of a sympathetic nerve action potential to the neurovascular junction initiates an intracellular cascade resulting in the release of noradrenaline and other co-transmitters [1]
● This study has examined differences in sympathetic transduction between normotensive and hypertensive males
● The main finding of this study is that men with untreated hypertension have lower sympathetic transduction compared to normotensive men of the same age
Summary
The arrival of a sympathetic nerve action potential to the neurovascular junction initiates an intracellular cascade resulting in the release of noradrenaline and other co-transmitters [1]. Abluminal receptors on the vascular smooth muscle transduce this signal, usually resulting in vasoconstriction through the activation of adrenoreceptors [2] This is a key mechanism by which the sympathetic nervous system (SNS) regulates arterial tone and arterial pressure in humans. How effectively the vasculature can react to sympathetic neural activity (SNA) is dependent on the various mechanisms that transduce the signal from the postganglionic nerve terminals to the contractile responses of the vasculature. Other vasoactive molecules such as endothelin, purines, or nitric oxide can modulate the efficacy of the SNA on vascular tone [3, 4]. Our group has created a novel analytical technique of measuring sympathetic transduction and has subsequently identified differences in the transduction of the SNA signal between both young and old individuals of both sexes [12]
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