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Reduced cerebral blood flow response and compensation among patients with untreated hypertension

From the University of Pittsburgh (Drs. Jennings, Muldoon, Ryan, Price, Sutton-Tyrrell, and Meltzer, P. Greer), PA; and University of Maastricht (Dr. van der Veen), the Netherlands.

Address correspondence and reprint requests to Dr Jennings, E1329 WPIC, 3811 O’Hara St., Pittsburgh, PA 15213; e-mail: JenningsJR{at}upmc.edu

Objective: To determine whether memory performance in hypertensive subjects induces diminished parietal and prefrontal blood flow activation relative to normotensive subjects but compensatory amygdala/hippocampal activation.

Methods: Thirty-seven untreated hypertensive subjects and 59 normotensive control subjects performed in two memory and one sensorimotor task while global and regional cerebral blood flow (rCBF) was assessed with [¹⁵O]water and PET. Neuropsychological, carotid artery ultrasound, and MRI assessments were obtained.

Results: When they were engaged in memory tasks, increases of CBF in hypertensive subjects were less than in normotensive subjects in the posterior parietal area, as expected; blunted responses were also shown within the middle posterior arterial watershed and thalamus. Relative to all other participants, hypertensive subjects that performed relatively well on verbal memory showed an enhanced rCBF response in the right amygdala/hippocampus. Furthermore, hypertensive, but not normotensive, subjects showed task-induced rCBF in the amygdala/hippocampal area that was significantly correlated with task-induced prefrontal rCBF. No confounding influences were identified from carotid artery or MRI measures.

Conclusions: Memory performance in hypertensive individuals is related to a blunted regional cerebral blood flow (rCBF) response, particularly in parietal cortex. Potentially compensatory rCBF responses appear to occur in midbrain and correlate with prefrontal rCBF.

Supported by grant NHLBI HL57529.

Presented in preliminary form at the Hypertension Council Meetings of the American Heart Association, Chicago, IL, 2002, and Washington, DC, 2003, and at the American Psychosomatic Society, Granada, 2001.

Received August 30, 3004. Accepted in final form December 27, 2004.

This article has been cited by other articles:

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