Selective α1-adrenergic blockade disturbs the regional distribution of cerebral blood flow during static handgrip exercise
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Selective α1-adrenergic blockade disturbs the regional distribution of cerebral blood flow during static handgrip exercise. / Fernandes, Igor A; Mattos, João D; Campos, Monique O; Machado, Alessandro C; Rocha, Marcos Paulo; Rocha, Natalia G; Vianna, Lauro C; Nobrega, Antonio C L.
In: American Journal of Physiology: Heart and Circulatory Physiology, Vol. 310, No. 11, 2016, p. H1541-H1548.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Selective α1-adrenergic blockade disturbs the regional distribution of cerebral blood flow during static handgrip exercise
AU - Fernandes, Igor A
AU - Mattos, João D
AU - Campos, Monique O
AU - Machado, Alessandro C
AU - Rocha, Marcos Paulo
AU - Rocha, Natalia G
AU - Vianna, Lauro C
AU - Nobrega, Antonio C L
N1 - Copyright © 2016 the American Physiological Society.
PY - 2016
Y1 - 2016
N2 - Handgrip-induced increases in blood flow through the contralateral artery that supplies the cortical representation of the arm have been hypothesized as a consequence of neurovascular coupling and a resultant metabolic attenuation of sympathetic cerebral vasoconstriction. In contrast, sympathetic restraint, in theory, inhibits changes in perfusion of the cerebral ipsilateral blood vessels. To confirm whether sympathetic nerve activity modulates cerebral blood flow distribution during static handgrip (SHG) exercise, beat-to-beat contra- and ipsilateral internal carotid artery blood flow (ICA; Doppler) and mean arterial pressure (MAP; Finometer) were simultaneously assessed in nine healthy men (27 ± 5 yr), both at rest and during a 2-min SHG bout (30% maximal voluntary contraction), under two experimental conditions: 1) control and 2) α1-adrenergic receptor blockade. End-tidal carbon dioxide (rebreathing system) was clamped throughout the study. SHG induced increases in MAP (+31.4 ± 10.7 mmHg, P < 0.05) and contralateral ICA blood flow (+80.9 ± 62.5 ml/min, P < 0.05), while no changes were observed in the ipsilateral vessel (-9.8 ± 39.3 ml/min, P > 0.05). The reduction in ipsilateral ICA vascular conductance (VC) was greater compared with contralateral ICA (contralateral: -0.8 ± 0.8 vs. ipsilateral: -2.6 ± 1.3 ml·min(-1)·mmHg(-1), P < 0.05). Prazosin was effective to induce α1-blockade since phenylephrine-induced increases in MAP were greatly reduced (P < 0.05). Under α1-adrenergic receptor blockade, SHG evoked smaller MAP responses (+19.4 ± 9.2, P < 0.05) but similar increases in ICAs blood flow (contralateral: +58.4 ± 21.5 vs. ipsilateral: +54.3 ± 46.2 ml/min, P > 0.05) and decreases in VC (contralateral: -0.4 ± 0.7 vs. ipsilateral: -0.4 ± 1.0 ml·min(-1)·mmHg(-1), P > 0.05). These findings indicate a role of sympathetic nerve activity in the regulation of cerebral blood flow distribution during SHG.
AB - Handgrip-induced increases in blood flow through the contralateral artery that supplies the cortical representation of the arm have been hypothesized as a consequence of neurovascular coupling and a resultant metabolic attenuation of sympathetic cerebral vasoconstriction. In contrast, sympathetic restraint, in theory, inhibits changes in perfusion of the cerebral ipsilateral blood vessels. To confirm whether sympathetic nerve activity modulates cerebral blood flow distribution during static handgrip (SHG) exercise, beat-to-beat contra- and ipsilateral internal carotid artery blood flow (ICA; Doppler) and mean arterial pressure (MAP; Finometer) were simultaneously assessed in nine healthy men (27 ± 5 yr), both at rest and during a 2-min SHG bout (30% maximal voluntary contraction), under two experimental conditions: 1) control and 2) α1-adrenergic receptor blockade. End-tidal carbon dioxide (rebreathing system) was clamped throughout the study. SHG induced increases in MAP (+31.4 ± 10.7 mmHg, P < 0.05) and contralateral ICA blood flow (+80.9 ± 62.5 ml/min, P < 0.05), while no changes were observed in the ipsilateral vessel (-9.8 ± 39.3 ml/min, P > 0.05). The reduction in ipsilateral ICA vascular conductance (VC) was greater compared with contralateral ICA (contralateral: -0.8 ± 0.8 vs. ipsilateral: -2.6 ± 1.3 ml·min(-1)·mmHg(-1), P < 0.05). Prazosin was effective to induce α1-blockade since phenylephrine-induced increases in MAP were greatly reduced (P < 0.05). Under α1-adrenergic receptor blockade, SHG evoked smaller MAP responses (+19.4 ± 9.2, P < 0.05) but similar increases in ICAs blood flow (contralateral: +58.4 ± 21.5 vs. ipsilateral: +54.3 ± 46.2 ml/min, P > 0.05) and decreases in VC (contralateral: -0.4 ± 0.7 vs. ipsilateral: -0.4 ± 1.0 ml·min(-1)·mmHg(-1), P > 0.05). These findings indicate a role of sympathetic nerve activity in the regulation of cerebral blood flow distribution during SHG.
KW - Adrenergic alpha-1 Receptor Antagonists/administration & dosage
KW - Adult
KW - Arterial Pressure
KW - Blood Flow Velocity
KW - Carotid Artery, Internal/innervation
KW - Cerebrovascular Circulation/drug effects
KW - Forearm
KW - Hand Strength
KW - Healthy Volunteers
KW - Humans
KW - Male
KW - Muscle Contraction
KW - Muscle, Skeletal/innervation
KW - Neurovascular Coupling/drug effects
KW - Prazosin/administration & dosage
KW - Receptors, Adrenergic, beta-1/drug effects
KW - Regional Blood Flow
KW - Sympathetic Nervous System/drug effects
KW - Time Factors
KW - Vasoconstriction/drug effects
KW - Young Adult
U2 - 10.1152/ajpheart.00125.2016
DO - 10.1152/ajpheart.00125.2016
M3 - Journal article
C2 - 27016578
VL - 310
SP - H1541-H1548
JO - American Journal of Physiology: Heart and Circulatory Physiology
JF - American Journal of Physiology: Heart and Circulatory Physiology
SN - 0363-6135
IS - 11
ER -
ID: 257930033