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.

Fig. 1. Correlation of age versus resting muscle sympathetic activity (MSNA), and sympathetic-vascular transduction.

MSNA versus age (NTN; r = 0.61; p = 0.0072) or untreated hypertension (uHTN; r = 0.52; p = 0.042). There is no difference between the slopes of the correlation between age and MSNA (p = 0.52).

Fig. 2. Example of data used to calculate sympathetic-vascular transduction in a hypertensive (HTN) and normotensive (NTN) male.

For each DBP the MSNA burst area was measured (area under the curve) in a two cardiac cycle window at a fixed lag of 6–8 cardiac cycles preceding the DBP for both participants. This ‘window’ was moved across the whole baseline file, associating each DBP with an MSNA burst area. These data were represented as a scatter plot. MSNA burst area was then binned into 1%/s bins, and the corresponding DBP (mean ± SD) plotted. A weighted linear regression was then fitted to these data, the slope of which gave our measurement of transduction (units of mmHg (%/s)). MSNA muscle sympathetic nerve activity, DBP diastolic blood pressure.

Fig. 3. Sympathetic-vascular transduction in men with normotension (NTN) and untreated hypertension (uHTN).

Mean ± standard deviation, **p = 0.0083.

Fig. 4. Correlations of sympathetic transduction to resting MSNA levels and age in both normotensive and untreated hypertensive men.

A correlation of sympathetic-vascular transduction to resting muscle sympathetic activity (MSNA) in men with normotension (NTN; r = 0.48; p = 0.16) or untreated hypertension (uHTN; r = 0.33; p = 0.23). When the groups were combined there was an inverse correlation between the two variables (r = −0.622; p = 0.006). B Sympathetic transduction versus age (NTN; r = 0.44; p = 0.038) or untreated hypertension (uHTN; r = 0.56; p = 0.03). There is no difference between the slopes of the correlation between age and sympathetic-vascular transduction (p = 0.99).