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. 2011 Jan;110(1):76-82.
doi: 10.1152/japplphysiol.00912.2010. Epub 2010 Nov 4.

Neurovascular responses to mental stress in prehypertensive humans

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Neurovascular responses to mental stress in prehypertensive humans

Christopher E Schwartz et al. J Appl Physiol (1985). 2011 Jan.

Abstract

Neurovascular responses to mental stress have been linked to several cardiovascular diseases, including hypertension. Mean arterial pressure (MAP), muscle sympathetic nerve activity (MSNA), and forearm vascular responses to mental stress are well documented in normotensive (NT) subjects, but responses in prehypertensive (PHT) subjects remain unclear. We tested the hypothesis that PHT would elicit a more dramatic increase of MAP during mental stress via augmented MSNA and blunted forearm vascular conductance (FVC). We examined 17 PHT (systolic 120-139 and/or diastolic 80-89 mmHg; 22 ± 1 yr) and 18 NT (systolic < 120 and diastolic < 80 mmHg; 23 ± 2 yr) subjects. Heart rate, MAP, MSNA, FVC, and calf vascular conductance were measured during 5 min of baseline and 5 min of mental stress (mental arithmetic). Mental stress increased MAP and FVC in both groups, but the increases in MAP were augmented (Δ 10 ± 1 vs. Δ14 ± 1 mmHg; P < 0.05), and the increases in FVC were blunted (Δ95 ± 14 vs. Δ37 ± 8%; P < 0.001) in PHT subjects. Mental stress elicited similar increases in MSNA (Δ7 ± 2 vs. Δ6 ± 2 bursts/min), heart rate (Δ21 ± 3 vs. Δ18 ± 3 beats/min), and calf vascular conductance (Δ29 ± 10 vs. Δ19 ± 5%) in NT and PHT subjects, respectively. In conclusion, mental stress elicits an augmented pressor response in PHT subjects. This augmentation appears to be associated with altered forearm vascular, but not MSNA, responses to mental stress.

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Figures

Fig. 1.
Fig. 1.
Changes (Δ) in systolic (SAP), diastolic (DAP), mean arterial pressures (MAP), and heart rate (HR) (expressed as both absolute and percent change) during 5 min of mental stress in normotensive (NT; n = 18) and prehypertensive (PHT; n = 16) subjects. Mental stress elicited a significant pressor response in both groups, and this response was augmented in PHT subjects. Mental stress increased HR in both NT and PHT subjects, and there was no significant difference between groups. Values are means ± SE. *P < 0.05 from corresponding NT value.
Fig. 2.
Fig. 2.
Changes in muscle sympathetic nerve activity (MSNA) bursts per minute and total MSNA during 5 min of mental stress in NT and PHT subjects. Mental stress increased MSNA burst frequency and total MSNA in both groups. These responses were not different between groups (burst frequency: time × group, P = 0.43; total MSNA: time × group, P = 0.29). Values are means ± SE. *P < 0.05 from baseline. N.S., no significance; a.u., arbitrary units per minute.
Fig. 3.
Fig. 3.
Changes in forearm blood flow (FBF), vascular resistance (FVR), and vascular conductance (FVC) during 5 min of mental stress. Mental stress elicited forearm vasodilation in both groups, but these responses were blunted in PHT (n = 15) compared with NT (n = 17) subjects (time × group = P < 0.01, all). Values are means ± SE. *P < 0.05 from baseline.
Fig. 4.
Fig. 4.
Changes in calf blood flow (CBF), vascular resistance (CVR), and vascular conductance (CVC) during 5 min of mental stress. Mental stress elicited calf vasodilation in NT (n = 17) and PHT (n = 14) groups, and these responses were not different between groups (time × group, P > 0.20, all). Values are means ± SE. *P < 0.05 from baseline.

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