Cardiovascular responsiveness to sympathoexcitatory stress in mild-hypertensive and normotensive participants

Autonomic dysfunction is implicated in cardiovascular disease, with studies reporting an exaggerated blood pressure response to sympathoexcitatory stress in individuals with resting hypertension (1-3). It is not clear whether this response is associated with changes in cardiac autonomic modulation or altered peripheral cardiovascular dynamics. The aim of this study was to compare blood pressure (BP), heart rate variability (HRV) and limb blood flow between normotensive (N: mean±SD; BP 116.9±1.4/73.4±0.9mmHg; age 49.4±10.4years, BMI 26.4±4.5kg.m-2; n=49) and mildly hypertensive participants (H: BP 141.3±2.0/88.8±2.2mmHg; age 51.7±11.4years, BMI 30.5±5.0kg.m-2; n=17) at rest and in response to sympathoexcitatory stress. Participants performed a cold pressor test (CPT) and an ischaemic handgrip test (IHGT) and were assessed for BP, forearm blood flow and HRV at rest and in response to the tests. Data are expressed as mean±SD and comparisons were made using ANOVA (SPSS Version 19, IBM Statistics, SPSS Inc., USA). The CPT evoked greater increases in systolic blood pressure (SBP; H: 18.13±13.01mmHg; N: 8.84±12.38mmHg; p=0.011) and mean arterial pressure (MAP; H: 10.13±9.55mmHg; N 4.65±8.16mmHg; p=0.026) in hypertensive compared with normotensive participants. The IHGT evoked greater increases in diastolic (DBP; H: 6.88±5.48mmHg; N: 0.32±7.20mmHg; p=0.001) and MAP (H: 9.24±4.85mmHg, N: 3.26±6.24mmHg; p=0.001) in hypertensive compared with normotensive participants. Hypertensive participants had significantly lower levels of resting cardiac parasympathetic modulations measured as the high frequency power of HRV (H: 31.7±4.1nu; N: 42.1±2.2nu; p=0.026). There were no significant differences in the HRV or blood flow responses to the CPT or IHGT between hypertensive and normotensive participants. This study demonstrated that sympathoexcitatory stress triggered an augmented blood pressure response in hypertensive participants, in line with previous studies (1-3). However, we found no evidence to support stress-activated hyper-reactivity in HRV or forearm blood flow in hypertensive participants. These findings lend support to the notion that sympathetic dominance contributes to the pathogenesis of hypertension. From the findings, we propose that more direct markers of autonomic function be investigated to better understand the role of the autonomic nervous system on the stress induced blood pressure response