Sympathetic-transduction in untreated hypertension

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.

Attenuated Sympathetic Blood Pressure Transduction in Patients With Treated Heart Failure With Reduced Ejection Fraction

“…Of note, higher resting MSNA also was associated with lower signal-averaged sympathetic-BP transduction in time-domain analyses involving both healthy young participants 22,39 and in patients with hypertension. 17 To exclude the possibility that such inverse relationships simply signal a flaw in the analytic method (ie, with high burst frequency there are fewer and shorter periods of the neural quiescence required to discriminate between BP changes after burst-associated and nonburst-associated cardiac cycles) 22,40,41 rather than an observation of functional hemodynamic importance, we conducted a subset analysis. Sympathetic-BP transduction was lower in the subgroup of participants with HFrEF whose resting MSNA burst frequency was similar to that of healthy controls.…”

“…Time-domain signal averaging, quantifying the BP changes subsequent to a discrete sympathetic burst, with consequent norepinephrine release and neurogenic vasoconstriction, is the method most commonly applied for this purpose. 15 This time-domain technique has been used to quantify differences in sympathetic transduction present in aging, 16 hypertension, 17 diabetes mellitus, 18 and obstructive sleep apnea, 19 but thus far a treated HFrEF population has not been examined.…”

Advances in pathogenesis and treatment of essential hypertension

“…MSNA plays a significant role in determining total peripheral resistance and vasoconstrictive function by controlling skeletal muscle (69). And MSNA may be a key cause of the huge individual variability in sympathetic hypertension, since studies have demonstrated that transduction of MSNA into vascular tone varies with age and sex (70,71), and there is a close association of MSNA with attended (observed) and unattended (unobserved) BP levels in essential hypertension (72). The manifestations of BP changes in sympathetic hypertension are also complex, including morning hypertension, nocturnal hypertension, sleep apnea-related hypertension, orthostatic hypertension, resistant hypertension, etc., which may all be associated with autonomic dysregulation (73).…”

Does COVID‐19 influence the sympathetic regulation of blood pressure?

“…2021). Meanwhile, Kobetic & colleagues (2021) recently reported lower sympathetic transduction in a sample of individuals with untreated hypertension compared with normotensive control subjects. Although Stute et al .…”