Plasma catecholamines

Drug withdrawal Stress (takotsubo) cardiomyopathy occurred in a 44-year-old man in whom severe opioid withdrawal was precipitated 2 hours after administration of naltrexone for alcohol consumption [117 ]. He had a history of heroin use and was taking methadone 120mg/day. Stress cardiomyopathy was beheved to be the result of a marked increase in catecholamine plasma concentrations following abrupt opioid withdrawal. 

Piaacidil has a short half-life and most human studies were carried out ia slow-release formulatioas. The reductioa ia blood pressure produced by piaacidil is accompanied by tachycardia and fluid retention. Plasma catecholamines and renin activity are iacreased. Other side effects are headache, di22iaess, and asthenia. 

Adrenaline (epinephrine) is a catecholamine, which is released as a neurotransmitter from neurons in the central nervous system and as a hormone from chromaffin cells of the adrenal gland. Adrenaline is required for increased metabolic and cardiovascular demand during stress. Its cellular actions are mediated via plasma membrane bound G-protein-coupled receptors. 

Mitsui, A., Nohta, H., and Ohkura, Y., High-performance liquid chromatography of plasma catecholamines using 1,2-diphenylethylenediamine as precolumn fluorescence derivatization reagent, /. Chromatogr., 344, 61, 1985. 

Multiple electrodes have been used to obtain selectivity in electrochemical detection. An early example involved the separation of catecholamines from human plasma using a Vydac (The Separation Group Hesperia, CA) SCX cation exchange column eluted with phosphate-EDTA.61 A sensor array using metal oxide-modified surfaces was used with flow injection to analyze multicomponent mixtures of amino acids and sugars.62 An example of the selectivity provided by a multi-electrode system is shown in Figure 2.63... 

Fenn, R. J., Siggia, S., and Curran, D. J., Liquid chromatography detector based on single and twin electrode thin-layer electrochemistry application to the determination of catecholamines in blood plasma, Anal. Client., 50, 1067,1978. 

Dutton, J., Hodgkinson, A. J., Hutchinson, G., and Roberts, N. B., Evaluation of a new method for the analysis of free catecholamines in plasma using automated sample trace enrichment with dialysis and HPLC, Clin. Chem., 45, 394, 1999. 

Robertson, D., Frolich, J., Carr, R., Watson, J., FFollifield, J., Shand, D., and Oates, J., Effects of caffeine on plasma renin activity, catecholamines, and blood pressure, New England Journal of Medicine, 298, 181, 1978. 

The neurotransmitters of the ANS and the circulating catecholamines bind to specific receptors on the cell membranes of effector tissue. Each receptor is coupled to a G protein also embedded within the plasma membrane. Receptor stimulation causes activation of the G protein and formation of an intracellular chemical, the second messenger. (The neurotransmitter molecule, which cannot enter the cell, is the first messenger.) The function of intracellular second messenger molecules is to elicit tissue-specific biochemical events within the cell that alter the cell s activity. In this way, a given neurotransmitter may stimulate the same type of receptor on two different types of tissue and cause two different responses due to the presence of different biochemical pathways within each tissue. 

The most common second messenger activated by protein/peptide hormones and catecholamines is cyclic adenosine monophosphate (cAMP). The pathway by which cAMP is formed and alters cellular function is illustrated in Figure 10.1. The process begins when the hormone binds to its receptor. These receptors are quite large and span the plasma membrane. On the cytoplasmic surface of the membrane, the receptor is associated with a G protein that serves as the transducer molecule. In other words, the G protein acts as an intermediary between the receptor and the second messengers that will alter cellular activity. These proteins are referred to as G proteins because they bind with guanosine nucleotides. In an unstimulated cell, the inactive G protein binds guanosine diphosphate (GDP). When the hormone... 

Some less obvious phenomena of catecholamine transport and biosynthesis further illustrate the complexities of deciphering how efferents from midbrain dopamine neurons contribute to sleep-wake regulation. The plasma membrane norepinephrine transporter (NET), which is responsible for the uptake of extracellular noradrenaline, can also readily transport dopamine, and does so in vivo. This... 

Kamimori G. H., Penetar D. M., Headley D. B. et al. (2000). Effect of three caffeine doses on plasma catecholamines and alertness during prolonged wakefulness. Eur. J. Clin. Pharmacol. 56, 537-44. 

Figure 15 Chromatograms of catecholamines obtained from (a) human and (b) Sprague-Dawley rat plasma. Peaks NE = norepinephrine E = epinephrine I = 3,4-dihydroxybenzylamine DA = dopamine. (From Ref. 88.)...

Copper is part of several essential enzymes including tyrosinase (melanin production), dopamine beta-hydroxylase (catecholamine production), copper-zinc superoxide dismutase (free radical detoxification), and cytochrome oxidase and ceruloplasmin (iron conversion) (Aaseth and Norseth 1986). All terrestrial animals contain copper as a constituent of cytochrome c oxidase, monophenol oxidase, plasma monoamine oxidase, and copper protein complexes (Schroeder et al. 1966). Excess copper causes a variety of toxic effects, including altered permeability of cellular membranes. The primary target for free cupric ions in the cellular membranes are thiol groups that reduce cupric (Cu+2) to cuprous (Cu+1) upon simultaneous oxidation to disulfides in the membrane. Cuprous ions are reoxidized to Cu+2 in the presence of molecular oxygen molecular oxygen is thereby converted to the toxic superoxide radical O2, which induces lipoperoxidation (Aaseth and Norseth 1986). 

Catecholamines from non-neuronal intracellular and extracellular sources can interact with cells of the immune system. Recently, NE and EPI that can be released by activating stimuli have been detected in lymphocytes and macrophages [reviewed in 2], These cells may synthesize catecholamines and/or take up and store catecholamines from extracellular sources (i.e., NE released from sympathetic nerves or NE and EPI present in the plasma). 

Nonimmune stresses can increase circulating proinflammatory cytokine concentrations. Hemorrhage, and certain psychological and physical stresses all increase HPA activity through mechanisms that may include catecholamines and peripheral CRH [reviewed in 29], However, in some experiments correlations between plasma ACTH and IL-6 levels in models of immune and nonimmune stresses are low. The role played by cytokines in the ACTH response to nonimmune stresses has not been established. 

Recent studies have shown that cyanide releases catecholamines from rat pheochromocytoma cells and brain slices (Kanthasamy et al. 1991b), from isolated bovine adrenal glands (Borowitz et al. 1988), and from the adrenals of mice following subcutaneous injection of high doses of potassium cyanide (Kanthasamy et al. 1991b). Thus, it was proposed that the cardiac and peripheral autonomic responses to cyanide are partially mediated by an elevation of plasma catecholamines (Kanthasamy et al. 1991b). 

Kanthasamy AG, Borowitz JL, Isom GE. 1991b. Cyanide-induced increases in plasma catecholamines Relationship to acute toxicity. Neurotoxicology 12 777-784. 

Disulfoton exposure altered catecholamine levels in animals, and this hormonal imbalance may be associated with elevated acetylcholine levels (Brzezinski 1969, 1972, 1973 Brzezinski and Ludwicki 1973 Brzezinski and Rusiecki 1970 Wysocka-Paruszewska 1970, 1971). In these studies, acute dosing with disulfoton caused increases in urinary and plasma noradrenaline and adrenaline levels, accompanied by decreases of adrenaline in the adrenal glands, in rats. In addition, the major urinary metabolite of catecholamine metabolism, 4-hydroxy-3-methoxymandelic acid (HMMA), was recovered in the urine from rats given acute doses of disulfoton (Wysocka-Paruszewska 1970,... 

The maximum level of HMMA in the urine occurred 72 hours after exposure, which coincides with the time period for maximum urine catecholamine levels. There was a direct relationship between blood cholinesterase inhibition and catecholamine (adrenaline and noradrenaline) levels in the urine and blood (Brzezinski and Ludwicki 1973). Maximum inhibition of cholinesterase activity and maximum plasma catecholamine occurred during the first I-2 hours after exposure. However, catecholamine levels returned to normal more rapidly than cholinesterase activity. It was proposed that high levels of acetylcholine, which are normally associated with cholinesterase activity inhibition, caused a release of catecholamines from the stores in the adrenals. 

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