Circulating norepinephrine and cerebrovascular control in conscious humans

• Published in: Clinical physiology and functional imaging 2003-11, Vol.23 (6), p.314-319
• Main Authors: Kimmerly, D. S., Tutungi, E., Wilson, T. D., Serrador, J. M., Gelb, A. W., Hughson, R. L., Shoemaker, J. K.
• Format: Article
• Language: English
• Subjects: Adult; alpha-adrenergic receptors; Blood Flow Velocity - drug effects; Blood Flow Velocity - physiology; Blood Pressure - drug effects; Blood Pressure - physiology; Brain - blood supply; Brain - drug effects; Brain - physiology; cerebral autoregulation; cerebral blood flow; Cerebrovascular Circulation - drug effects; Cerebrovascular Circulation - physiology; Consciousness - drug effects; Consciousness - physiology; Dose-Response Relationship, Drug; Female; Hemostasis - drug effects; Hemostasis - physiology; Humans; Infusions, Intravenous; Male; Middle Cerebral Artery - drug effects; Middle Cerebral Artery - physiology; Norepinephrine - administration & dosage; Norepinephrine - blood; phentolamine; Phentolamine - administration & dosage; transcranial Doppler; Vasoconstriction - drug effects; Vasoconstriction - physiology
• ISSN: 1475-0961; 1475-097X
• DOI: 10.1046/j.1475-0961.2003.00507.x

Summary Background:  Cerebral vasoconstriction without concurrent changes in systemic arterial blood pressure has been observed in both normal individuals and those with idiopathic orthostatic intolerance following several minutes of postural stress when circulating catecholamines are elevated. Therefore, we tested the hypothesis that α‐adrenergic activation with and without elevated circulating norepinephrine (NE) directly affects cerebrovascular tone in healthy individuals. Methods:  Mean arterial pressure (MAP; tonometry) and cerebral blood flow velocity (MFV) in the middle cerebral artery (transcranial Doppler) were measured in seven healthy individuals during 15 min periods of saline and of 50 (low NE) and 100 (high NE) ng kg−1 min−1 infusions of NE. Following this, phentolamine (PHO) was administered to return MAP back to baseline while high NE infusion continued (high NE + PHO). Finally, NE infusion was stopped allowing the persistent effects of PHO to dominate. Results:  Circulating NE caused a dose‐dependent increase in MAP (P