Norepinephrine urinary

Kawano Y., Kawasaki T., Kawazoe N. et al. (1990). Circadian variations of urinary dopamine, norepinephrine, epinephrine and sodium in normotensive and hypertensive subjects. Nephron 55(3), 277-82. 

More specific laboratory tests are used to diagnose secondary hypertension. These include plasma norepinephrine and urinary metanephrine levels for pheochromocytoma, plasma and urinary aldosterone levels for primary aldosteronism, and plasma renin activity, captopril stimulation test, renal vein renins, and renal artery angiography for renovascular disease. 

The stress of cold produced increased urinary excretion of norepinephrine but not of epinephrine or vasopressin (K8). Cold in the form of accidental hypothermia also resulted in increased serum creatine phos-phokinase (M2). Mental stress (problem solving) resulted in increases of urinary vasopressin from 33 to 47.6 units, epinephrine from 5.5 to 11.3 mg, and norepinephrine from 17 to 21 mg (K8). 

K8. Konzett, H., Hortnagl, H., and Winkler, K., On the urinary output of vasopressin, epinephrine and norepinephrine during different stress situations. Psy-chopharmacologia 21, 247-256 (1971). 

The initial report of sustained, lower urinary cortisol levels in PTSD highlighted the disassociation between cortisol and catecholamine levels in PTSD. Norepinephrine and epinephrine levels assayed from the same urine specimens revealed elevations in both of these catecholamines, while cortisol levels in PTSD fell within the normal range of 20-90 pg/day, indicating that the alteration was not in the hypoadrenal or endocrinopathologic range (Mason et al. 1986). This finding established the expectation that alterations in basal levels of cortisol might be subtle, and not easily differentiated from normal values (Mason et al. 1986). 

The detrusor muscle (which contains (32-adrenoceptors) in the body of the urinary bladder is relaxed by epinephrine and isoproterenol. On the other hand, the trigone and sphincter (which contain aj-receptors) are contracted by norepinephrine and epinephrine this action inhibits the voiding of urine. 

The TCA drugs have lost their place as first-line therapy for depression because of their bothersome side effects (Table 33.2) at therapeutic doses and lethal effects in toxic doses. In addition to their presynaptic effects on the neuronal uptake of norepinephrine and serotonin, they block several postsynaptic receptors. They are potent cholinergic muscarinic receptor antagonists, resulting in symptoms such as dry mouth, constipation, tachycardia, blurred vision and urinary retention. Blockade of histamine receptors (Hi) often results in sedation and weight gain. Antagonism of aj-adrenoceptors in the vasculature can cause orthostatic hypotension. 

Mechanism of Action A sympathomimetic amine that produces CNS and respiratory stimulation, mydriasis, bronchodilation, a pressor response, and contraction of the urinary sphincter Directly effects alpha and beta receptor sites in peripheral system. Enhancesreleaseof norepinephrine by blocking reuptake, inhibiting monoamine oxidase. Therapeutic Effect Increases motor activity, mental alertness decreases drowsiness, fatigue. 

The involvement of the noradrenergic pathways may be one of the mechanisms by which stressors influence tic severity. For example, a series of adult TS patients were found to have elevated levels of cerebrospinal fluid (CSF) norepinephrine (Leckman et ah, 1995) and to have excreted high levels of urinary norepinephrine in response to the stress of lumbar puncture (Chappell et ah, 1994). These elevated levels of CSF norepinephrine may also contribute to the elevation in CSF corticotopin-releasing factor levels seen in some TS patients (Chappell et ah, 1996). 

Ravindran AV, Bialik RJ, Lapierre YD Primary early onset dysthymia, biochemical correlates of the therapeutic response to fluoxetine, 11 urinary metabolites of serotonin, norepinephrine and melatonin. J Affect Disord 31 119-123, 1994d Razani J, White KL, White J, et al The safety and efficacy of combined amitryptiline and tranylcypromine antidepressant treatment—a controlled trial. Arch Gen Psychiatry 40 657-661, 1983... 

Low 24-hour urinary 3-methoxy-4-hydroxy- phenylglycol (metabolite of norepinephrine), primarily in bipolar disorders (i.e., depressed phase)... 

Also of interest is the report by Anderson and colleagues (154) that found a reduction in the urinary output of norepinephrine and its metabolites in nine female SAD patients treated with light therapy. They concluded that the results were compatible with changes seen after antidepressant drug therapy and recommended controlled trials to confirm this preliminary finding. 

Atropine and other antimuscarinic drugs have been used to provide symptomatic relief in the treatment of urinary urgency caused by minor inflammatory bladder disorders (Table 8-3). However, specific antimicrobial therapy is essential in bacterial cystitis. In the human urinary bladder, M2 and M3 receptors are expressed predominantly with the M3 subtype mediating direct activation of contraction. As in intestinal smooth muscle, the M2 subtype appears to act indirectly by inhibiting relaxation by norepinephrine and epinephrine. 

Intravenous administration of dopamine promotes vasodilation of renal, splanchnic, coronary, cerebral, and perhaps other resistance vessels, via activation of Di receptors. Activation of the Di receptors in the renal vasculature may also induce natriuresis. The renal effects of dopamine have been used clinically to improve perfusion to the kidney in situations of oliguria (abnormally low urinary output). The activation of presynaptic D2 receptors suppresses norepinephrine release, but it is unclear if this contributes to cardiovascular effects of dopamine. In addition, dopamine activates Bj receptors in the heart. At low doses, peripheral resistance may decrease. At higher rates of infusion, dopamine activates vascular a. receptors, leading to vasoconstriction, including in the renal vascular bed. Consequently, high rates of infusion of dopamine may mimic the actions of epinephrine. 

Pheochromocytoma is a tumor of the adrenal medulla or sympathetic ganglion cells. The tumor secretes catecholamines, especially norepinephrine and epinephrine. The patient in the case study at the beginning of the chapter had a left adrenal pheochromocytoma that was identified by imaging. In addition, she had elevated plasma and urinary norepinephrine, epinephrine, and their metabolites, normetanephrine and metanephrine. 

The catecholamines are a group of hormones secreted by the adrenal medulla. The major urinary metabolite of norepinephrine and epinephrine is vanillylmandelic acid (VMA). Urinary levels of VMA are considerably higher than those of total catecholamine. From the standpoint of laboratory methodology, VMA estimation is preferable to total catecholamine estimation, although it is not a simple procedure. VMA has been shown to be elevated in some patients who had phenochromocytoma and normal urinary catecholamines, even though patients with neuroblastoma have a normal VMA level and elevated catecholamine levels. 

Since dopamine is present in sympathetic nervous tissue as a precursor of norepinephrine, and it has a separate metabolic pathway that yields homovanillic acid (HVA), tumors such as neuroblastomas may cause elevations of the urinary dopamine and its metabolite HVA. In some cases these elevations have been observed with normal VMA, total catecholamine, and metanephrine. Urinary HVA is usually normal in patients with phenochromocytoma. Increased HVA is found in special fluids of patients with Parkinson s disease treated with L-dopa. 

Two parallel groups of healthy volunteers received 20 mg of citalopram (n = 12) or placebo (n = 6) once daily for 10 d in a randomized, double-blind fashion, followed by concomitant selegiline, 10 mg once daily for 4 d. The safety of this drug combination was assessed by measurements of blood pressure, heart rate, body temperature, and inquiries for adverse events. Blood samples were taken for the analysis of serum concentrations of selegiline, citalopram, and their metabolites. In addition, plasma was obtained to measure prolactin, epinephrine, norepinephrine, and 3,4-dihydroxyphanolglycol (DHPG), the urinary excretion of norepinephrine and 5-hydroindoleacetic acid (5-HIAA), the urinary metabolite of serotonin. 

The human uterus contains and B2 receptors. The fact that the Breceptors mediate relaxation may be clinically useful in pregnancy (see Clinical Pharmacology). The bladder base, urethral sphincter, and prostate contain receptors that mediate contraction and therefore promote urinary continence. The specific subtype of ai receptor involved in mediating constriction of the bladder base and prostate is uncertain, but uia receptors probably play an important role. The B2 receptors of the bladder wall mediate relaxation. Ejaculation depends upon normal a-receptor (and possibly purinergic receptor) activation in the ductus deferens, seminal vesicles, and prostate. The detumescence of erectile tissue that normally follows ejaculation is also brought about by norepinephrine (and possibly neuropeptide Y) released from sympathetic nerves. Alpha activation appears to have a similar detumescent effect on erectile tissue in female animals. 

Dalmaz, Y. and Peyrin, L., Rapid procedure for chromatographic isolation of DOPA, DOPAC, epinephrine, norepinephrine and dopamine from a single urinary sample at endogenous levels, J. Chromatogr., 145, 11, 1978 Chem. Abs., 88, 59809c, 1978. 

Atomoxetine increases the brain concentrations of norepinephrine. Adverse effects (constipation, dry mouth, nausea, fatigue, decreased appetite, insomnia, chest pain, palpitations, anxiety, erectile dysfunction, mood swings, nervousness and urinary retention) are more common in poor metabolizers of CYP2D6, as atomoxetine is metabolized through the cytochrome CYP2D6 pathway. 

Dexamphetamine sulphate acts by stimulating the release of norepinephrine and dopamine from storage sites and may also slow down the metabolism of catecholamines by inhibiting MAO. Usually about 30% is excreted unchanged in the urine this urinary excretion reaches 60% when the urine is acidic (pH 5.5-6). It is metabolized by cytochrome P450. 

Norepinephrine increases in parts of fhe brain and body and at receptors other than those that cause therapeutic actions (e.g., unwanted actions of norepinephrine on acefyichoiine reiease causing decreased appefife, increased heart rate and biood pressure, dry mouth, urinary retention, etc.)... 

Urinary retention in men over 50 with borderline urine flow has been observed with other agents with potent norepinephrine reuptake blocking properties (e.g., reboxetine, milnacipran), so administer atomoxetine with caution to these patients... 

Most of the evidence supporting the biogenic amine hypothesis is indirect. Specifically, deficits of norepinephrine and/or serotonin have been cUfficult to demonstrate. Considerable research into urinary levels of methoxy-hydroxy-phenylethanolamine glycol (MHPG), a norepinephrine metaboUte, in depressed... 

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