Dopamine urinary

Dopamine 0.5—10+ mcg/kg per minute BP, HR, urinary output and kidney function, ECG, extremity perfusion (higher doses only)... 

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. 

Wang et al. injected a Texas-red-labelled phosphorothioated AS-ODN into the dopamine lA receptor in the rat renal interstitium. Fluorescence was detected after 24 h in both tubular epithelium and intra-renal vasculature. Treatment resulted in a 35% decrease in the dopamine lA receptor protein, causing a reduction in urinary sodium excretion and urine output [131],... 

Pharmacokinetics Non-ergot dopamine agonists are rapidly absorbed. The absolute bioavailability is more than 90%. Steady-state concentrations are achieved within 2 days of dosing. Terminal half-life is about 8 hours (about 40 minutes for apomorphine) in young healthy volunteers and about 12 hours in elderly volunteers. Urinary excretion is the major route of elimination. 

Dysfunction of the dopamine system has been implicated in autism. Abnormalities have been observed in levels of whole blood, urinary and CSF dopamine and HVA. Also dopamine antagonists alleviate some autistic symptoms. It is thought that the levels of the HVA in the CSF reflect central... 

Similar to findings in animal models of early-life stress, elevated 24-hour urinary NE, epinephrine (E), and dopamine (DA) excretion as well as decreased platelet adrenergic receptors have been measured in abused children with PTSD (Perry, 1994 DeBellis et al., 1999a). Abused children with PTSD also exhibit... 

Randrup et al. (55) first postulated a role for dopamine in depressive disorders. More recently, a reanalysis of the data from several groups has found evidence for a bimodal distribution of CSF homovanillic acid (HVA) levels in depressed patients, with one group comparable with normal control subjects and the other with decreased levels (56). Roy and colleagues (57) also reported on the potential predictive value of lower urinary HVA output in depressed patients who attempted suicide versus those who did not. Both reports indicate a decreased turnover in dopamine. 

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. 

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. 

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. 

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. 

Trim C M, Moore J N, Clark E S 1989 Renal effects of dopamine infusion in conscious horses. Equine Veterinary Journal 7(suppl) 124-128 Watson E D, McGorum B C, Keeling N et al 1997 Oestrogen respronsive urinary incontinence in two mares. Equine Veterinary Education 9 81-84 Wilcox C S 1991 Diuretics. In Brenner B M, Rector F C (eds) The kidney, 4th edn. Saunders, Philadelphia, PA, pp. 2123-2147... 

Dopamine. Dopamine is u.scd in the treatment of shock. It is ineffective orally, in large part because it is a substrate for both MAO and COMT. Thus, it is used intravenously. In contrast with the catecholamines NE and epinephrine, dopamine increases blood flow to the kidney in doses that have no chronotropic effect on the heart or that cause no increa.se in blood pressure, lire increased blood How to the kidneys enhances glomerular filtration rate, Na excretion, and. in turn, urinary output. The dilation of renal blood ve.s-.sels produced by dopamine is the result of its agonist action on the D -dopaminc receptor. 

In contrast to production of VMA, production of homovanillic acid (HVA) from dopamine depends mainly on 0-methylation of the deaminated metabohte of dopamine, 3,4-dihydroxyphenylacetic acid (DOPAC), and to a lesser extent on deamination of methoxytyramine, the O-methylated metabohte of dopamine (Figure 29-4). As a result, HVA is formed in multiple tissues, with about 30% of circulating and urinary HVA arising from mesenteric organs and up to 20% from the brain. 

In humans, VMA and the sulfates and glucuronide conjugates of MHPG represent the main end products of norepinephrine and epinephrine metabolism (Table 29-1). HVA and conjugates of HVA are the main metabolic end products of dopamine metabolism. These end products and the other conjugates are eliminated mainly by urinary excretion. As a result, their circulatory clearance is slow and plasma concentrations high relative to those of the precursor amines. 

Peripheral Dopaminergic System Dopamine is usually thought of as a neurotransmitter in the brain or as an intermediate in the production of norepinephrine and epinephrine in the periphery. It has been presumed tliat these sources account for the large amounts of dopamine and dopamine metabolites excreted in urine. The contribution of the brain to circulating levels and urinary excretion of dopamine metabolites is, however, now known to be relatively minor. Also, in sympathetic nerves and the adrenal medulla most dopamine is converted to norepinephrine. Therefore other sources and functions of dopamine in the periphery must be considered. Emerging evidence suggests the presence of a third peripheral catecholamine system, in which dopamine functions not as a neurotransmitter or circulating hormone, but as an autocrine or paracrine substance. ... 

Although the kidneys represent the major source of urinary free dopamine, this source does not account for the larger amounts of excreted dopamine metabolites, such as HVA and dopamine sulfate. Findings of large arterial-to-portal venous increases in plasma concentrations of dopamine and its metabolites have indicated that substantial amounts of dopamine are produced and metabolized in the GI tract and otlier mesenteric organs. ... 

---