title: Conjugated catecholamines in human plasma: where are they coming from?
abstract: The origins of conjugated catecholamines remain poorly known. The aim of the present study was to see whether a major contribution comes from the sympathetic nervous system. We have assumed some kind of parallelism between the activity of the sympathetic nervous system, the amount of catecholamines released and taken up, and the amount of conjugated catecholamines circulating in plasma. Accordingly, an increase in sympathetic activity should be followed by an increase in the plasma level of conjugated catecholamines. The plasma levels of sulfoconjugated and glucuroconjugated catecholamines were measured in 10 patients with mental disease resistant to drug treatment, before and after electroconvulsive therapy. As expected, blood pressure, norepinephrine concentration, and epinephrine concentration in plasma were transiently increased. Neither sulfoconjugated nor glucuroconjugated catecholamines were significantly changed. Conjugated catecholamines were measured in 10 volunteers before and at the nadir of insulin-induced hypoglycemia. As expected, plasma levels of norepinephrine and epinephrine were drastically increased. Plasma levels of sulfoconjugates were decreased and glucuroconjugates increased; these were narrow but statistically significant variations. Data reported in the present article do not support a major role for the activity of the sympathetic system in fixing the level of conjugated catecholamines in human plasma. This is a negative, but nonetheless important, observation. In human subjects, currently available information suggests an important role for the intestinal wall and renal function in determining the level of circulating sulfoconjugates.
authors.affiliation: Clinical Pharmacology Laboratory, Faculty of Medicine, Paris, France.
authors.forename: J L
authors.initials: JL
authors.lastname: Cuche
authors.forename: P
authors.initials: P
authors.lastname: Brochier
authors.forename: N
authors.initials: N
authors.lastname: Klioua
authors.forename: M F
authors.initials: MF
authors.lastname: Poirier
authors.forename: H
authors.initials: H
authors.lastname: Cuche
authors.forename: M
authors.initials: M
authors.lastname: Benmiloud
authors.forename: H
authors.initials: H
authors.lastname: Loo
authors.forename: M
authors.initials: M
authors.lastname: Safar
mesh_terms: D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure; D002395:Catecholamines / Q000097:blood*; D004565:Electroconvulsive Therapy; D004837:Epinephrine / Q000031:analogs & derivatives / Q000097:blood; D005965:Glucuronates / Q000097:blood*; D006801:Humans; D007003:Hypoglycemia / Q000097:blood / Q000139:chemically induced; D007328:Insulin; D001523:Mental Disorders / Q000097:blood / Q000628:therapy; D009638:Norepinephrine / Q000031:analogs & derivatives / Q000097:blood; D013431:Sulfates / Q000097:blood*; D013564:Sympathetic Nervous System / Q000502:physiology*
chemical_list: D001786:Blood Glucose; D002395:Catecholamines; D005965:Glucuronates; D007328:Insulin; D013431:Sulfates; C046910:norepinephrine glucuronide; C046911:epinephrine glucuronide; C036526:epinephrine sulfate; C017574:noradrenaline sulfate; D009638:Norepinephrine; D004837:Epinephrine