Premium
Forearm vascular conductance during mental stress is predicted by the hemodynamic response but not arterial catecholamines
Author(s) -
Pike Tasha Lynn,
RamirezMarrero Farah,
Welch Brian T.,
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.a877-a
Subject(s) - medicine , brachial artery , hemodynamics , forearm , blood pressure , cardiology , vasodilation , haemodynamic response , mean arterial pressure , heart rate , surgery
The forearm blood flow response to mental stress (MS) is due to circulating epinephrine (Epi), release of nitric oxide, and forearm sympathetic withdrawal. We recently demonstrated that forearm venous Epi predicts the vascular conductance (FVC) and HR response to MS. In a large, ongoing phenotyping study of sympathoexcitation and adrenergic receptor gene variation, we hypothesized that arterial Epi would predict the forearm vasodilator response to MS, while norepinephrine (NE) would predict the pressor response. In 54 healthy, normotensive young adults, FVC (plethysmography), HR (ECG), and blood pressure (brachial artery) were measured in a recumbent chair at rest and during 3 min of a computerized Stroop colored‐word test. During the final 30 sec of stress, arterial Epi and NE were assayed (HPLC). MS increased HR, BP, FVC, Epi, and NE (p < 0.05 for all). Unexpectedly, during MS the arterial Epi levels did not correlate with HR or FVC. However, a robust correlation existed for HR and FVC (r = 0.73, p < 0.001). Further, systolic pressure correlated with FVC (r = 0.36, p < 0.01) and NE (r = 0.46, p < 0.001). We conclude that the HR response to MS is a major contributor to FVC, independent of arterial Epi, suggestive of mechanical effects and potentially flow‐mediated dilation. This also confirms previous work that catecholamine spillover assays are more indicative of sympathoadrenal activation and hemodynamic responses. Support: K23 RR17520, HL 46493.