Cardiovascular haemodynamic response to repeated mental stress in normotensive subjects at genetic risk of hypertension: evidence of enhanced reactivity, blunted adaptation, and delayed recovery.

Abstract

To identify unique cardiovascular responses to stressors in a population at genetic risk of hypertension, we studied haemodynamic responses in initial reactivity to, subsequent adaptation to, and final recovery from repeated active mental stress in young, normotensive individuals stratified by hypertension parental history (PH). Two groups (n=21/group) of normotensive white males underwent stress testing. One group (N+PH) had a hypertensive parent, while the other group (N-PH) did not. Cardiovascular response was measured before, during, and after repeated serial-subtraction math. Initial reactivity was measured as the difference between baseline and initial stress response, subsequent adaptation as the difference in response to repeated trials, and final recovery was assessed by the difference between baseline and postbaseline levels. The influence of PH on reactivity, adaptation, and recovery was assessed by repeated measures ANOVA for stroke volume, cardiac output, pre-ejection period, total peripheral resistance, mean successive heartbeat time difference, blood pressure, and heart rate. Multivariate analysis of variance (MANOVA) determined the effect of PH on overall reactivity, adaptation, and recovery. As compared to the N-PH group, initial reactivity was higher in the N+PH group for cardiac index (P<0.05) and pre-ejection period (P<0.05). Subsequent adaptation in the N+PH group was significantly slower for pre-ejection period (P=0.03). Finally, the N+PH group showed delayed recovery in heart rate (P=0.03), diastolic blood pressure (P<0.05), and pre-ejection period (P=0.007). In conclusion, the heightened reactivity, lack of adaptation, and delayed recovery occur in the sympathetic system of normotensive subjects at genetic risk of hypertension, specifically in beta-adrenergic responses (pre-ejection period). The parasympathetic response (mean successive heartbeat time difference) was not different. Increased cardiac output reactivity in the N+PH group (P<0.05) thus precedes any difference in blood pressure reactivity (P<0.99). Delayed recovery of diastolic blood pressure is also found in the N+PH group (P<0.05), which suggests lower baroreceptor sensitivity. Since delayed recovery in heart rate (P=0.03), and diastolic blood pressure (P<0.05) occur in N+PH subjects even before the corresponding changes in reactivity (P>0.10) or adaptation (P>0.07) are seen, these recovery impairments may be among the earliest precursors to the development of essential hypertension in this population. Finally, PH group haemodynamic differences suggest that these traits (reactivity, adaptation, and recovery) may constitute early 'intermediate' phenotypes in the pathogenesis of hypertension.