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Ambulatory arterial stiffness index (AASI) does not predict baroreflex sensitivity or the pressor response to mental stress in normotensive humans
Author(s) -
Liu Zhong,
Hesse Christiane,
Pike Tasha L.,
Issa Amine,
Restrepo Miguel Bernal,
Charkoudian Nisha,
Joyner Michael J.,
Eisenach John H.
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a879-b
Subject(s) - arterial stiffness , baroreflex , cardiology , medicine , baroreceptor , blood pressure , ambulatory , ambulatory blood pressure , heart rate , diastole , mean arterial pressure
Ambulatory arterial stiffness index (AASI) is a novel measure of arterial stiffness, which independently predicts cardiovascular mortality, even in nomortensive subjects. Baroreflex sensitivity (BRS) is integral to BP regulation, and varies among healthy persons. Baroreceptors sense arterial pressure indirectly from the degree of stretch of the elastic arterial walls. A reduced ability of baroreflex buffering in elderly, hypertensives, and patients with carotid denervation results in an elevated pressor response to mental stress (MS). We hypothesized that there might be a correlation between BRS and AASI in healthy subjects, and individuals with higher BRS would have a lower pressor response to MS. We measured 24‐hour ambulatory BP, BRS (modified Oxford), HR, and intra‐arterial pressure (AP) during MS in 53 healthy, normotensive, non‐obese individuals (32 women, 21 men, mean age ± SE: 28 ± 1). AASI was defined as 1 minus the regression slope plotted from diastolic over systolic BP using all of the ambulatory BP readings. Although all measures were widely variable among subjects, there was no relationship between AASI, BRS, or pressor response to MS. We conclude that in the absence of aging, cardiovascular, or autonomic disease, the novel stiffness index (AASI) and baroreflex control of heart rate are unable to account for the complex pressor response to MS. Support: K23 RR17520, HL 46493, DFG grant He 4605/1‐1.