Selective α1-adrenergic blockade disturbs the regional distribution of cerebral blood flow during static handgrip exercise

• Published in: American journal of physiology. Heart and circulatory physiology 2016-06, Vol.310 (11), p.H1541-H1548
• Main Authors: Fernandes, Igor A, Mattos, João D, Campos, Monique O, Machado, Alessandro C, Rocha, Marcos P, Rocha, Natalia G, Vianna, Lauro C, Nobrega, Antonio C L
• Format: Article
• Language: English
• Subjects: Adrenergic alpha-1 Receptor Antagonists - administration & dosage; Adult; Arterial Pressure; Blood Flow Velocity; Carotid Artery, Internal - innervation; Cerebrovascular Circulation - drug effects; Forearm; Hand Strength; Healthy Volunteers; Humans; Male; Muscle Contraction; Muscle, Skeletal - innervation; Neurovascular Coupling - drug effects; Prazosin - administration & dosage; Receptors, Adrenergic, beta-1 - drug effects; Receptors, Adrenergic, beta-1 - metabolism; Regional Blood Flow; Sympathetic Nervous System - drug effects; Sympathetic Nervous System - metabolism; Time Factors; Vasoconstriction - drug effects; Young Adult
• ISSN: 1522-1539
• DOI: 10.1152/ajpheart.00125.2016

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.