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Functional Assessment of Urinary Neuro-biogenic Amines—A COMPREHENSIVE GUIDE 


Goldstein, David S (2010)

Catecholamines 101.

Clinical autonomic research : official journal

of the Clinical Autonomic Research

Society vol. 20 (6) p. 331-52

Jong, Wilhelmina H. A. de; Eisenhofer,

Graeme; Post, Wendy J.; Muskiet, Frits A.

J.; Vries, Elisabeth G. E. de et al. (2013)

Dietary Influences on Plasma and Urinary

Metanephrines: Implications for

Diagnosis of Catecholamine-Producing


Endocrine Society

Oeltmann, Timothy; Carson, Robert;

Shannon, John R.; Ketch, Terry;

Robertson, David (2004)

Assessment of O-methylated catecholamine

levels in plasma and urine for diagnosis

of autonomic disorders

Autonomic Neuroscience vol.

116 (1) p. 1-10

Vialou, V.; Balasse, L.; Dumas, S.; Giros, B.;

Gautron, S. (2007)

Neurochemical characterization of pathways

expressing plasma membrane mono-

amine transporter in the rat brain


vol. 144 (2) p. 616-622

Yalcin, Emine B.; More, Vijay; Neira, Karissa

L.; Lu, Zhenqiang James; Cherrington,

Nathan J. et al. (2013)

Downregulation of Sulfotransferase

Expression and Activity in Diseased

Human Livers

Drug Metab. Dispos.

vol. 41 (9) p. 1642-1650


Small amounts of epinephrine are

constantly secreted to maintain normal

blood pressure and metabolic functions.

Evidence is accumulating that epineph-

rine has neurotransmitter-like functions

in the CNS that may affect the regula-

tion of blood pressure, respiration, and

pituitary hormone secretion.

Clinically, plasma epinephrine lev-

els have been shown to reflect central

nervous system (CNS) neural outflow

to the adrenal medulla. Virtually all cir-

culating epinephrine originates from the

adrenal medulla.



epinephrine levels may

occur in conditions such as Addision’s

disease, diabetic nephropathy, con-

genital 21-hydroxylase deficiency and

Autonomic Failure syndromes. Alpha-

and beta-blocker medications may re-

duce the effects of epinephrine, but

are not documented to reduce systemic

epinephrine levels. Metyrosine therapy

decreases levels of the precursor neu-

rotransmitters dopamine and norepi-

nephrine, and may reduce epinephrine



or elevated levels of epineph-

rine may be secreted during acute stress

(fight or flight response). Short-term

stress-response elevations increase heart

rate, blood pressure, muscle strength and

blood glucose levels, and decrease insu-

lin levels, parasympathetic and diges-

tive functions. Virtually all circulating

epinephrine present during the “stress

response” originates from the adrenal

medulla. Epinephrine elevations have

been documented in extreme exercise,

panic attacks and some cases of essen-

tial hypertension. Plasma epinephrine

levels have been shown to elevate in re-

sponse to global metabolic threats, such

as shock (hypoglycemia, hemorrhagic

hypotension, asphyxia, circulatory col-

lapse) and also during emotional dis-

tress. Serious illness and stress can cause

moderate to large temporary increases in

catecholamine levels.




(POTS) patients may have elevat-