Catecholamines test

If a series of related chemicals, say noradrenaline, adrenaline, methyladrenaline and isoprenaline, are studied on a range of test responses (e.g. blood pressure, heart rate, pupil size, intestinal motility, etc.) and retain exactly the same order of potency in each test system, then it is likely that there is only one type of receptor for all four of these catecholamines. On the other hand, if, as Ahlquist first found in the 1940s, these compounds give a distinct order of potency in some of the tests, but the reverse (or just a different) order in others, then there must be more than one type of receptor for these agonists. 

In all tested organisms, PCBs — especially PCBs with 2,3,7,8-TCDD-like activity — adversely affected patterns of survival, reproduction, growth, metabolism, and accumulation. Common manifestations of PCB exposure in animals include hepatotoxicity (hepatomegaly, necrosis), immunotox-icity (atrophy of lymphoid tissues, suppressed antibody responses), neurotoxicity (impaired behavior and development, catecholamine alterations), increased abortion, low birth weight, embryolethality, teratogenicity, gastrointestinal ulceration and necrosis, bronchitis, dermal toxicity (chloracne, edema,... 

Other components of the urine are conjugates with sulfuric acid, glucuronic acid, glycine, and other polar compounds that are synthesized in the liver by biotransformation (see p. 316). In addition, metabolites of many hormones (catecholamines, steroids, serotonin) also appear in the urine and can provide information about hormone production. The proteohormone chorionic gonadotropin (hCG, mass ca. 36 kDa), which is formed at the onset of pregnancy, appears in the urine due to its relatively small size. Evidence of hCG in the urine provides the basis for an immunological pregnancy test. 

Oral contraceptives have their most significant effect on endocrine parameters. Blood cortisol, thyroxine, protein-bound iodine, T3 uptake, and urinary free cortisol are elevated. Urinary 17,21-dihydroxy steroids, 17-ketosteroids, and estrogens are decreased. There is no effect on urinary catecholamines or VMA (Table 10) (LIO). The effect of thyroid functions tests is due to the administered hormone stimulating an increase in the production of thyroid-binding globulin which in turn binds 1-thyroxine. The lowering of free thyroxine stimulates the anterior pituitary to produce thyrotropin, which in turn stimulates the thyroid to produce more thyroxine. Since the additional thyroxine is bound to the extra protein, there is an equilibrium and the patient remains clinically euthyroid, but the protein-bound iodine and the thyroxine are elevated. 

Drug/Lab test interactions A labetalol metabolite may falsely increase urinary catecholamine levels when measured by a nonspecific trihydroxyindole reaction. Drug/Food interactions Food may increase bioavailability of the drug. 

Drug/Lab test interactions Methyidopa may interfere with tests for Urinary uric acid by phosphotungstate method serum creatinine by alkaline picrate method AST by colorimetric methods. Because methyidopa causes fluorescence in urine samples at the same wavelengths as catecholamines, falsely high levels of urinary catecholamines may occur and will interfere with the diagnosis of pheochromocytoma. 

Drug/Lab test interactions The antianabolic action of tetracyclines may cause an increase in blood urea nitrogen. During doxycycline or minocycline therapy, false elevations of urinary catecholamine levels may occur... 

Methenamine mandelate, 1 g four times daily, or methen-amine hippurate, 1 g twice daily by mouth (children, 50 mg/kg/d or 30 mg/kg/d, respectively), is used only as a urinary antiseptic to suppress, not treat, urinary tract infection. Acidifying agents (eg, ascorbic acid, 4-12 g/d) may be given to lower urinary pH below 5.5. Sulfonamides should not be given at the same time because they may form an insoluble compound with the formaldehyde released by methenamine. Persons taking methenamine mandelate may exhibit falsely elevated tests for catecholamine metabolites. 

Cocaine [50-36-2] - [ALKALOIDS] (Vol 1) - [ALKALOIDS] (Vol 1) -and catecholamines [EPINEPHRINE AND NOREPINEPHRINE] (Vol 9) -forensic testing for [FORENSIC CHEMISTRY] (Vol 11) -substance abuse of [PSYCHOPHARMACOLOGICAL AGENTS] (Vol 20)... 

Method for catecholamines by HPLC. A few microlitres of a 10 3-Af solution of dopamine, norepinephrine or similar compounds are transferred to a small test-tube and diluted to 20 jul with 0.05 M sodium phosphate (pH 8) at 4 °C [ 102]. 10 jul of a 0.2% solution of fluorescamine in acetone are then added with vigorous shaking. An aliquot portion of this mixture is applied directly to the HPLC column. The derivatives are separated on Hitachi 3011 or 3010-OH gels (column, 50 cm X 3 mm) with methanol-0.05 M Tris-hydrochloric acid buffer of pH 8 (7 3) at room temperature at a flow-rate of 0.72 ml/min. The separation of fluorescamine derivatives of dopamine and norepinephrine with this system is shown in Fig.4.52. 

When making a choice of test situations, some investigators are biased by the effects of the tested substance in adulthood. Based on this knowledge, it is possible to formulate and test a specific hypothesis about aspects of brain and behavioral development that are expected to be affected. For instance, haloperidol can be expected to alter development of the dopamine system and motor activity, whereas clonidine can be expected to affect development of the catecholamine system and REM sleep. 

Murray and coauthors (Murray et al. 2001) claim that corticotropin-releasing hormones, catecholamines, neuropeptides, and steroid hormones produced throughout the central nervous system as well as in several peripheral sites including the pituitary, testes, ovaries, heart, adrenals, and immune tissues play an important role in the immunomodulatory mechanism of stress affecting human or animal bodies. 

In the safety pharmacology protocol, the interaction of multiple endocrine systems in test animals is addressed. As discussed by Harvey (1996) and by Harvey and Everett (2003), effects on adrenocortical function are frequently found in toxicology studies, sometimes related to enzyme induction and effects on steroid biosynthesis (Loose et al. 1983, Nebert and Russell 2002, Weber et al. 1993). Test procedures in animals are required when there is a reason for concern. Frequently however the effects observed are due to stress rather than specific interaction with the target organ, and may involve effects on catecholamine release from the adrenal medulla (Tucker 1996). Recently, much new evidence has been accumulated from the testing of industrial chemicals with effects on adrenal steroid biosynthesis (Harvey and Johnson 2002). 

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