Effects of Mental Stress and Slow Breathing on Autonomic Control of Arterial Blood Pressure (ABP) in Young Normotensives with Hypertensive Parents (FH+) Relative to Those with Normotensive Parents (FH‐)

Abstract

Young normotensive (FH+) have greater risk of hypertension than FH-. Whether mental stress differentially affects autonomic control of ABP in young normotensive FH+ relative to FH- and whether slow breathing might reduce risk of hypertension in FH+ is not known.In 25 FH- and 23 FH+ (aged 18-25 years), we recorded ABP, ECG and respiratory frequency (Rf); Stroke volume (SV), cardiac output (CO) and total peripheral resistance (TPR) were derived from the pulse contour. The vagal component of baroreflex sensitivity (BRS) was tested by the sequence method at rest and during mental stress (Colour Stroop test). The vagosympathetic BRS was recorded as change in R-R interval evoked by the depressor response to stand from squat before and 0, 3, 6 min after mental stress. Heart rate variability (HRV) was analysed in time- and frequency-domains. Comparisons within and between FH- and FH+ were made by paired and unpaired t-tests. FH- and FH+ had similar mean ABP (ABP: 85±0.8 vs 88±1.8 mmHg) and Rf (15.9±0.6 vs 15.9±0.5 breaths/min) at rest. Mental stress increased ABP, HR, and Rf in both FH+ and FH-, but the increase in ABP was greater in FH+ (ABP: 82.0±2.0 to 109.0±4.0*; 78.3±1.8 to 98.5±2.2*†mmHg, respectively, *: P<0.05 within group, †: P<0.05 between groups). Further, CO increased in FH- only (FH-: 4.9±0.2 to 5.6±0.3*; FH+: 4.9±0.2 to 5.2±0.4 L/min), whereas TPR increased in FH+ only (FH-: 1.0±0.04 to 1.2±0.1; FH+: 1.1±0.1 to 1.8±0.3* units). Meanwhile, in the frequency domain, sympathetic indices increased and vagal indices of HRV decreased (LF increased, HF fell; LF/HF increased) in both FH- and FH+; vagal indices also decreased in the time domain (RMSSD: 60.5±7.2 to 46.8±4.8ms*; 65.8±7.9 to 47.7±6.7ms*, respectively). BRS decreased in mental stress during up- and down-sequences in SP in both FH- and FH+. Further, following the stress test, tachycardic BRS during squat to stand was preserved in FH+, but attenuated in FH- (0.50±0.05 to 0.29±0.07*; 0.50±0.05 to 0.47±0.07ms/mmHg respectively). Considering slow breathing, ABP decreased in both FH- and FH+ (ABP: 78.3±1.8 to 76.1±2.0*; 82.0±2.0 to 79.4±1.9*mmHg, respectively). Further, BRS during up-sequences increased in FH+ (0.98±0.09 to 1.2±0.09*ms/mmHg) to equal that of FH- (1.16±0.06 to 1.2±0.07ms/mmHg), while vagal indices of HRV increased and sympathetic indices decreased in FH- and FH+ (Log HF:1.7±0.03 to 1.93±0.01*; 1.7±0.03 to 1.94.01*, Log LF: 0.78±0.06 to 0.38±0.08*; 0.8±0.05 to 0.28±0.06*ms2). These findings suggest that young normotensive FH+ show an exaggerated pressor response to mental stress relative to FH- that is associated with enhanced sympathetic vasoconstriction in FH+. Further, although the vagal component of HRV and BRS was attenuated during mental stress in FH+ and FH-, the persistent tachycardic baroreflex for several minutes after stress in FH+ but not FH- suggests further baroreflex sympathetic activation can still occur in FH+. Such autonomic disturbances would be expected to increase future risk of hypertension in FH+. However, our findings with slow breathing suggest regular slow breathing may reduce this risk in FH+ by increasing cardiac vagal tone and reducing sympathetic tone.