The present study tested whether individuals who differ in the magnitude of their blood pressure reactions to a behavioral stressor also differ in their stressor-induced patterns of functional neural activation.
Sixteen participants (7 men, 9 women aged 47 to 72 years) were classified as high (n = 8) or low (n = 8) blood pressure reactors by the magnitude and temporal consistency of their systolic blood pressure (SBP) reaction to a Stroop color-word interference stressor. Both high and low SBP reactors completed this Stroop stressor while their task-related changes in blood pressure and functional neural activity were assessed in a blocked functional magnetic resonance imaging design.
In both high and low SBP reactors, the Stroop-stressor engaged the anterior cingulate, orbitofrontal, insular, posterior parietal, and the dorsolateral prefrontal regions of the cortex, the thalamus, and the cerebellum. Compared with low reactors, however, high reactors not only showed a larger magnitude increase in SBP to the Stroop stressor, but also an increased activation of the posterior cingulate cortex.
A behavioral stressor that is used widely in cardiovascular reactivity research, the Stroop stressor, engages brain systems that are thought to support both stressor processing and cardiovascular reactivity. Increased activation of the posterior cingulate, a brain region implicated in vigilance to the environment and evaluative emotional processes, may be a functional neural correlate of an individual's tendency to show large-magnitude (exaggerated) blood pressure reactions to behavioral stressors.
BMI = body mass index; BOLD = blood oxygen level dependent; DBP = diastolic blood pressure; fMRI = functional magnetic resonance imaging; MANOVA = multivariate analysis of variance; RF = radiofrequency; ROI = region of interest; SBP = systolic blood pressure; TE = time to echo; TR = time to repetition; VAS = visual analog scale.
From the Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, PA.
Received for publication May 31, 2004; revision received September 22, 2004.
Address correspondence and reprint requests to Peter J. Gianaros, Cardiovascular Behavioral Medicine Program, University of Pittsburgh, 3811 O'Hara Street, Pittsburgh, PA 15213. E-mail: email@example.com
This research was supported by an NHLBI-NRSA (1-F32–71333–01), an NIMH-MRSDA (1-K01-MH-070616–01), and by pilot funds awarded through the Pittsburgh Mind-Body Center at the University of Pittsburgh and Carnegie Mellon University (NIH HL65111 and HL65112) to Peter J. Gianaros.