TY - JOUR
T1 - Brachial artery responses to acute hypercapnia
T2 - The roles of shear stress and adrenergic tone
AU - Carr, Jay M.J.R.
AU - Ainslie, Philip N.
AU - Howe, Connor A.
AU - Gibbons, Travis D.
AU - Tymko, Michael M.
AU - Steele, Andrew R.
AU - Hoiland, Ryan L.
AU - Vizcardo-Galindo, Gustavo A.
AU - Patrician, Alex
AU - Brown, Courtney V.
AU - Caldwell, Hannah G.
AU - Tremblay, Joshua C.
N1 - Publisher Copyright:
© 2022 The Authors. Experimental Physiology © 2022 The Physiological Society.
PY - 2022/9/16
Y1 - 2022/9/16
N2 - New Findings: What is the central question of this study? What are the contributions of shear stress and adrenergic tone to brachial artery vasodilatation during hypercapnia? What is the main finding and its importance? In healthy young adults, shear-mediated vasodilatation does not occur in the brachial artery during hypercapnia, as elevated α₁-adrenergic activity typically maintains vascular tone and offsets distal vasodilatation controlling flow. Abstract: We aimed to assess the shear stress dependency of brachial artery (BA) responses to hypercapnia, and the α₁-adrenergic restraint of these responses. We hypothesized that elevated shear stress during hypercapnia would cause BA vasodilatation, but where shear stress was prohibited (via arterial compression), the BA would not vasodilate (study 1); and, in the absence of α₁-adrenergic activity, blood flow, shear stress and BA vasodilatation would increase (study 2). In study 1, 14 healthy adults (7/7 male/female, 27 ± 4 years) underwent bilateral BA duplex ultrasound during hypercapnia (partial pressure of end-tidal carbon dioxide, +10.2 ± 0.3 mmHg above baseline, 12 min) via dynamic end-tidal forcing, and shear stress was reduced in one BA using manual compression (compression vs. control arm). Neither diameter nor blood flow was different between baseline and the last minute of hypercapnia (P = 0.423, P = 0.363, respectively) in either arm. The change values from baseline to the last minute, in diameter (%; P = 0.201), flow (ml/min; P = 0.234) and conductance (ml/min/mmHg; P = 0.503) were not different between arms. In study 2, 12 healthy adults (9/3 male/female, 26 ± 4 years) underwent the same design with and without α₁-adrenergic receptor blockade (prazosin; 0.05 mg/kg) in a placebo-controlled, double-blind and randomized design. BA flow, conductance and shear rate increased during hypercapnia in the prazosin control arm (interaction, P < 0.001), but in neither arm during placebo. Even in the absence of α₁-adrenergic restraint, downstream vasodilatation in the microvasculature during hypercapnia is insufficient to cause shear-mediated vasodilatation in the BA.
AB - New Findings: What is the central question of this study? What are the contributions of shear stress and adrenergic tone to brachial artery vasodilatation during hypercapnia? What is the main finding and its importance? In healthy young adults, shear-mediated vasodilatation does not occur in the brachial artery during hypercapnia, as elevated α₁-adrenergic activity typically maintains vascular tone and offsets distal vasodilatation controlling flow. Abstract: We aimed to assess the shear stress dependency of brachial artery (BA) responses to hypercapnia, and the α₁-adrenergic restraint of these responses. We hypothesized that elevated shear stress during hypercapnia would cause BA vasodilatation, but where shear stress was prohibited (via arterial compression), the BA would not vasodilate (study 1); and, in the absence of α₁-adrenergic activity, blood flow, shear stress and BA vasodilatation would increase (study 2). In study 1, 14 healthy adults (7/7 male/female, 27 ± 4 years) underwent bilateral BA duplex ultrasound during hypercapnia (partial pressure of end-tidal carbon dioxide, +10.2 ± 0.3 mmHg above baseline, 12 min) via dynamic end-tidal forcing, and shear stress was reduced in one BA using manual compression (compression vs. control arm). Neither diameter nor blood flow was different between baseline and the last minute of hypercapnia (P = 0.423, P = 0.363, respectively) in either arm. The change values from baseline to the last minute, in diameter (%; P = 0.201), flow (ml/min; P = 0.234) and conductance (ml/min/mmHg; P = 0.503) were not different between arms. In study 2, 12 healthy adults (9/3 male/female, 26 ± 4 years) underwent the same design with and without α₁-adrenergic receptor blockade (prazosin; 0.05 mg/kg) in a placebo-controlled, double-blind and randomized design. BA flow, conductance and shear rate increased during hypercapnia in the prazosin control arm (interaction, P < 0.001), but in neither arm during placebo. Even in the absence of α₁-adrenergic restraint, downstream vasodilatation in the microvasculature during hypercapnia is insufficient to cause shear-mediated vasodilatation in the BA.
KW - autonomic control
KW - blood flow
KW - carbon dioxide
KW - vascular function
UR - http://www.scopus.com/inward/record.url?scp=85138674257&partnerID=8YFLogxK
U2 - 10.1113/EP090690
DO - 10.1113/EP090690
M3 - Article
C2 - 36114662
AN - SCOPUS:85138674257
SN - 0958-0670
VL - 107
SP - 1440
EP - 1453
JO - Experimental Physiology
JF - Experimental Physiology
IS - 12
ER -