Heightened Functional Neural Activation to Psychological Stress Covaries With Exaggerated Blood Pressure Reactivity

Abstract

Abstract-Individuals who show exaggerated blood pressure reactions to psychological stressors are at increased risk for hypertension, atherosclerosis, and stroke. We tested whether individuals who show exaggerated stressor-induced blood pressure reactivity also show heightened stressor-induced neural activation in brain areas involved in controlling the cardiovascular system. In a functional MRI study, 46 postmenopausal women (mean age: 68.04; SD: 1.35 years) performed a standardized Stroop color-word interference task that served as a stressor to increase blood pressure. Across individuals, a larger task-induced rise in blood pressure covaried with heightened and correlated patterns of activation in brain areas implicated previously in stress-related cardiovascular control: the perigenual and posterior cingulate cortex, bilateral prefrontal cortex, anterior insula, and cerebellum. Entered as a set in hierarchical regression analyses, activation values in these brain areas uniquely predicted the magnitude of task-induced changes in systolic (⌬R 2 ϭ0.54; PϽ0.001) and diastolic (⌬R 2 ϭ0.27; PϽ0.05) blood pressure after statistical control for task accuracy and subjective reports of task stress. Heightened stressor-induced activation of cingulate, prefrontal, insular, and cerebellar brain areas may represent a functional neural phenotype that characterizes individuals who are prone to show exaggerated cardiovascular reactivity. Key Words: blood pressure Ⅲ cardiovascular reactivity Ⅲ cerebellum Ⅲ cingulate Ⅲ insula Ⅲ orbitofrontal cortex Ⅲ psychological stress A cute psychological stress raises blood pressure in most individuals. A stress-induced rise in blood pressure results from autonomic-and neuroendocrine-mediated changes in cardiac contractility and peripheral vascular resistance. 1 These stressor-induced physiological changes are thought to provide metabolic support for adaptive behavior (eg, the "fight-or-flight" response). 2 Some individuals, however, have a tendency to show exaggerated rises in blood pressure that exceed the metabolic demands of psychological stressors. 3 Such exaggerated stressor-induced blood pressure reactions predict increased risk for hypertension, 4 stroke, 5 and preclinical atherosclerosis. 6,7 Blood pressure reactions to psychological stress are centrally controlled by brain systems that both cognitively process psychological stressors and coordinate autonomic, neuroendocrine, and cardiovascular activity with adaptive behavior. 8,9 Key among these brain systems are subdivisions of the cingulate, orbitofrontal, and insular cortices. 8 -15 Anatomically, subdivisions of the cingulate, orbitofrontal, and insular cortices can control peripheral physiology by reciprocal neural connections with cell groups in subcortical and brain stem areas that regulate autonomic, neuroendocrine, and cardiovascular activity. 8 -15 To date, however, it has not yet been established whether individuals who show exaggerated stressor-induced blood pressure reactivity also show greater stressor-induced neur...

A Brain Phenotype for Stressor‐Evoked Blood Pressure Reactivity

“…This stressor‐battery controls for individual differences in task engagement and motor responding through performance titration procedures. We have also found, in previous work, that cardiovascular and behavioral responding to tasks of this battery is reliable across neuroimaging and laboratory‐based testing contexts 31. Accordingly, it may be appropriate for developing stress reactivity norms across a variety of populations.…”

“…To compute prestressor BP and HR, the final 3 measurements from the prestressor period were averaged. The incongruent condition—minus—resting BP/HR change scores (ΔBP, ΔHR) were used to compute cardiovascular reactivity to match our previous work 31, 32. These change (reactivity) scores averaged over the Stroop and MSIT tasks were used in analyses given the high correlations between task reactivity scores (Figure 1).…”

Right anterior cingulate cortical volume covaries with respiratory sinus arrhythmia magnitude in combat veterans

“…Critchley, Gianaros, and their colleagues have been especially active in this area [36][37][38][39][40]. Using positron emission tomography (PET), Critchley et al observed in six participants that regional cerebral blood flow (rCBF) in the right dorsal ACC (Brodmann's areas 32 and 24) and right posterior insular cortex covaried directly with mean arterial pressure (MAP) during physical and mental challenge [36].…”

“…In this study, positive covariation with MAP was also exhibited by activations in dorsolateral prefrontal cortex (PFC); supplementary motor area; and sections of temporal, parietal, and occipital cortices. In a follow-up study of 46 postmenopausal women, Gianaros et al demonstrated that, across individuals, those participants with larger blood pressure responses exhibited larger BOLD activations in left pregenual ACC (in this case, anterior portions of Brodmann's area 32, excluding area 24), left insula, and right posterior cingulate cortex (Brodmann's area 31) [38].…”

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“…Gao et al found that the lateral cerebellar output (dentate) nucleus is not activated by the control of movement per se, but is strongly engaged during passive and active sensory tasks (Gao et al, 1996). Recent research of the cerebellum's contribution to cognitive processing and emotional processing have increased enormously, showing that the cerebellum is responsible for sensory perception, learning, memory, attention, linguistic, emotional control and conflict resolution processing (Mandolesi et al, 2001;Bischoff-Grethe et al, 2002;Vokaer et al, 2002;Claeys et al, 2003;Guenther et al, 2005;Allen et al, 2005;Konarski et al, 2005;Schmahmann & Caplan, 2006;Gianaros et al, 2007;Schweizer et al, 2007). Anatomical studies revealed that via the thalamus, the cerebellum interacts with multiple areas of the prefrontal cortex and subcortex limbic lobe (Middleton & Strick, 2001;Zhu et al, 2006).…”