Production and Excretion of Dopamine by the Isolated Perfused Rat Kidney

Adam, W. R.; Adams, Beverlie A.

doi:10.1159/000173048

Cited by 12 publications

(11 citation statements)

References 21 publications

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“…Earlier studies have demonstrated an increase in U DA V after administration of L-tyrosine or L-DOPA, both in the isolated perfused kidney (Buu et al 1986) and in vivo (Agharanya and Wurtman 1982;Buu et al 1985;Kaufman et al 1989). In contrast, Adam and Adams (1985) reported an effect of L-DOPA but not of L-tyrosine on U DA V in the isolated perfused kidney. This might have been due to the lower doses of catecholamine precursors used in the latter study.…”

Section: Discussionmentioning

confidence: 85%

Renal response to infusion of dopamine precursors in anaesthetized rats

Mühlbauer¹,

Gleiter²,

Gies³

et al. 1997

Naunyn-Schmiedeberg's Arch Pharmacol

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In the present study the renal response to intravenous infusion of the catecholamine precursors L-dihydroxyphenylalanine (L-DOPA) or L-tyrosine was investigated in thiopentone sodium-anaesthetized Sprague-Dawley rats. Glomerular filtration rate (GFR) was assessed by renal clearance of inulin, urinary concentration of dopamine (U(DA)V) by HPLC and sodium excretion (U(Na)V) by flame photometry. We found that basal U(DA)V was 6.5 +/- 0.5 pmol/min per 100 g body weight (mean +/- SEM). Intravenous infusion of L-tyrosine at 0. 1-3.0 micromol/min dose dependently enhanced U(DA)V (17 +/- 3 to 144 +/- 14 pmol/min respectively) with higher doses of L-tyrosine resulting in no further increase in U(DA)V. Compared with L-tyrosine administration significantly lower doses of L-DOPA (0.07 to 35 nmol/min) caused increases in U(DA)V which were orders of magnitude higher (18 +/- 1 to 7800 +/- 470 pmol/min, respectively) and did not show saturation characteristics. GFR did not change in response to L-tyrosine or L-DOPA infusion. No variations in urinary flow rate or in U(Na)V could be observed which were significantly correlated to changes in U(DA)V. In contrast, intravenous infusion of dopamine at a dose of 6 nmol/min significantly increased GFR by 35 +/- 6.2% and urinary flow rate by over 2-fold. Immunohistochemistry with light microscopy revealed no tyrosine hydroxylase in the kidney. Therefore, dopamine synthesis in the tubular cells mainly depends on the renal supply of L-DOPA. The unchanged GFR and U(Na)V in spite of large variations of U(DA)V argue against the hypothesis that intratubular dopamine plays a functional role in the regulation of hemodynamics or sodium transport in the kidney. Renal dopamine excretion may rather represent an effective pathway for the elimination of catecholamine precursors from the plasma.

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Section: Discussionmentioning

confidence: 85%

Renal response to infusion of dopamine precursors in anaesthetized rats

Mühlbauer¹,

Gleiter²,

Gies³

et al. 1997

Naunyn-Schmiedeberg's Arch Pharmacol

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“…However, there is evidence that both in humans and rats, decarboxylation of L-DOPA is not the only source of urine DA-and other endogenous sources are likely involved. In rats, DA urinary excretion was reduced but not totally abolished by inhibition of L-DOPA decarboxylase, fasting or sucrose by feeding (Cottet-Emard et al, 1980;Stephenson et al, 1982;Adam and Adams, 1985).…”

Section: Discussionmentioning

confidence: 93%

“…A number of cells are able to take up directly DA or its precursor L-DOPA, which is then converted into DA and its metabolites. This pathway has been emphasized in the renal tubules, but holds true also for the gastrointestinal tract and other tissues (as lungs) containing a variety of cells belonging to the APUD system (enterochromaffin cells, mast cells, etc) (Fujita, 1977;Landsberg et al, 1973;Baines and Chan, 1980;Adam and Adams, 1985). The extent to which decarboxylation of circulating L-DOPA contributes to urinary DA excretion is unclear.…”

Section: Discussionmentioning

confidence: 99%

Differential effect of guanethidine on dopamine and norepinephrine pools in urine, heart and superior cervical ganglion in the rat

Favre¹,

Haut²,

Boudet³

et al. 1987

J. Neural Transmission

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The time-related changes of dopamine (DA) and norepinephrine (NE) pools were investigated in heart, superior cervical ganglion (SCG) and urine in rats treated chronically with guanethidine (50 mg/kg i.p. five days each week). The efficiency of sympathectomy was assessed by the great loss of NE in heart and superior cervical ganglion (SCG) (-96% and -76% respectively of control values on day 18) together with the ready reduction of NE and 3-methoxy-4-hydroxyphenylglycol (MHPG) in urine. The pattern of changes was quite different for DA, which was less readily affected and at a lesser extent than NE in heart and SCG thus suggesting the presence of norepinephrine-independent DA stores. Similarly the urinary excretion of free DA, free 3,4-dihydroxyphenylacetic acid (DOPAC) and free homovanillic acid (HVA) was slightly decreased only from the 9th day, whereas urinary conjugated DA remained unaltered. These results indicate that the greatest portion of urine free and conjugated DA, free DOPAC and free HVA derives from peripheral pools located outside noradrenergic neurons. Alternatively, the time-course of DA sensitivity to guanethidine suggests that a portion of urine DA may originate from DA stored independently from NE in noradrenergic neurons.

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“…INC. that renal nerves release both norepinephrine and dopamine, and results of other studies suggest that dopamine dilates arteries in the rat renal cortex (Chapman et al, 1979). However, most evidence suggests that there are no dopaminergic nerves in the rat kidney, so the perivascular nerve plexuses described above probably are noradrenergic (Adam and Adams, 1985;McGrath et al, 1983). …”

mentioning

confidence: 94%

Catecholamine‐containing, dopamine‐beta‐hydroxylase‐immunoreactive perivascular nerve specializations in the rat kidney

et al. 1989

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Fluorescence histochemical visualization of catecholamines and immunolabeling of dopamine beta hydroxylase (DBH) were employed to study noradrenergic nerve terminals and perivascular nerve specializations in the rat kidney. Plexuses of catecholamine-containing and dopamine-beta-hydroxylase-immunoreactive nerves innervate the intrarenal arterial tree and larger intrarenal veins. Some perivascular nerve bundles have specialized segments composed of clusters of axonal enlargements that are immunoreactive for DBH and fluoresce intensely in ultraviolet light after fixation in a solution of formaldehyde and glutaraldehyde or treatment with glyoxylic acid. No fluorescent neural structures were found in denervated rat kidney sections treated with glyoxylic acid. Many such structures are associated with arteriolar branches of interlobar, arcuate, and interlobular arteries and are composed, in part, of axonal enlargements that contain mitochondria, microtubules, and one or more clusters of synaptic vesicles. These perivascular nerve specializations may be sites of axoaxonal interactions between noradrenergic axons or between these axons and other types of autonomic or sensory axons. The synaptic vesicles evidently store large amounts of catecholamine, but there is no evidence whether it is released into the surrounding tissue. These structures may be involved in changes in intrarenal innervation patterns which may occur as the rat ages. Regardless of the autonomic or sensory nature of intrarenal neural structures, close association of most such structures with arterioles suggests some neurovascular interaction.

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Production and Excretion of Dopamine by the Isolated Perfused Rat Kidney

Cited by 12 publications

References 21 publications

Renal response to infusion of dopamine precursors in anaesthetized rats

Renal response to infusion of dopamine precursors in anaesthetized rats

Differential effect of guanethidine on dopamine and norepinephrine pools in urine, heart and superior cervical ganglion in the rat

Catecholamine‐containing, dopamine‐beta‐hydroxylase‐immunoreactive perivascular nerve specializations in the rat kidney

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