The actions of dopamine and of sulpiride on regional blood flows in the rat kidney.

Chapman, B.J.; Horn, N M; Munday, K. A.; Robertson, Mark

doi:10.1113/jphysiol.1980.sp013093

Cited by 62 publications

(31 citation statements)

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“…Dopamine is synthesized within the kidney (1) and acts locally to produce natriuresis (2-5) and vasodilation (6). Although these roles for dopamine in kidney physiology are well established, the cellular localization of renal dopamine receptors has not been defined.…”

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confidence: 99%

Dopamine- and cAMP-regulated phosphoprotein (DARPP-32) and dopamine DA1 agonist-sensitive Na+,K+-ATPase in renal tubule cells.

Meister

Fryckstedt

Schalling

et al. 1989

Proc. Natl. Acad. Sci. U.S.A.

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The cellular localization of DARPP-32, a dopamine-and cAMP-regulated phosphoprotein of Mr 32,000 that appears to mediate certain actions of dopamine in the mammalian brain by acting as an inhibitor of protein phosphatase 1, was studied in the kidney of several species. DARPP-32 mRNA and DARPP-32-like inmunoreactivity were found in the cytoplasm of cells in the thick ascending limb of the loop of Henle. The specific dopamine DA, agonist SKF 82526 caused a dose-dependent inhibition ofNa+,K+-ATPase activity, which could be blocked by SCH 23390, a specific DA, antagonist, and by PKI-(5-24) amide, a specific inhibitor of cAMP-dependent protein kinase. The results indicate that DA1 dopamine receptors and DARPP-32, an intracellular third messenger for dopamine, are part of the signal-transduction process for dopamine acting on renal tubule cells.The neurotransmitter dopamine may play an important role in control of renal function. Dopamine is synthesized within the kidney (1) and acts locally to produce natriuresis (2-5) and vasodilation (6). Although these roles for dopamine in kidney physiology are well established, the cellular localization of renal dopamine receptors has not been defined.DARPP-32, a dopamine-and cAMP-regulated phosphoprotein with an apparent molecular weight of 32,000 by SDS/PAGE, has been purified from cytosol of bovine caudate nucleus (7,8). The complete amino acid sequence of bovine brain DARPP-32 has been determined (9), and its cDNA has been isolated and sequenced (10). In the central nervous system, DARPP-32 has been shown to be localized to dopaminoceptive cells containing the D1 dopamine receptor (11,12). It appears to serve as an intracellular third messenger mediating the actions of dopamine at these receptors (7,8,(11)(12)(13). Thus, the phosphorylation of DARPP-32 in intact nerve cells is increased by dopamine acting on D1 receptors, stimulation of adenylate cyclase, formation of cAMP, and stimulation of cAMP-dependent protein kinase (7,8). DARPP-32, in its phosphorylated form, is a potent inhibitor of phosphoprotein phosphatase 1 (14) and has amino acid sequence homology with phosphatase inhibitor 1 (I-1), also an inhibitor of phosphatase 1 (9).DARPP-32 has been analyzed primarily in the central nervous system. However, DARPP-32-like immunoreactivity has been detected in brown fat cells in pig (15), and the protein has been identified and purified from bovine adipose tissue (16). Previous studies have also identified DARPP-32 in ciliary epithelium (17) and in adrenal chromaffin cells, parathyroid cells, and choroid plexus (13). Evidence has been obtained for the presence of D1-like receptors in several of these tissues (18)(19)(20)(21)(22). Thus, DARPP-32 appears to be a useful marker for cells containing the central (D1) and peripheral (DA1) dopamine receptors. In the present study we investigated the cellular localization of DARPP-32 and, for purposes of comparison, I-1, in the kidney. Both proteins were localized in the same cells of a specific portion of the loop of Henle; ...

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mentioning

confidence: 99%

Dopamine- and cAMP-regulated phosphoprotein (DARPP-32) and dopamine DA1 agonist-sensitive Na+,K+-ATPase in renal tubule cells.

Meister

Fryckstedt

Schalling

et al. 1989

Proc. Natl. Acad. Sci. U.S.A.

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“…Keywords: renal haemodynamics, kidney function, natriuresis, dopamine, dose-response, tubular function, lithium clearance, sodium hydronephrotic kidney of the rat [4], thus supporting the Introduction concept of a vasodilating effect of specific dopaminergic D 1 -receptor activation, which at higher doses is opposed by In anaesthetized dogs [1] and rats [2], low doses of dopamine decreased renal vascular resistance, whereas higher doses an action of a-adrenergic receptors [5,6]. Another important effect of dopamine, which does not occur with other caused vasoconstriction.…”

Section: Aimsmentioning

confidence: 82%

“…a-adrenergic receptor blockade abolished the vasoconstriction so that vasodilation was catecholamines, is the increase in sodium excretion [5][6][7]. Stimulation of D 1 -receptors in proximal tubular brushobserved with all doses of dopamine [2]. These dosedependent effects have been confirmed in studies using border membranes inhibits the Na …”

Section: Aimsmentioning

confidence: 92%

“…The results suggest that the natriuretic effect of depressor doses of dopamine was primarily caused by attenuation of the increase in distal sodium reabsorption normally seen after an increase in proximal tubular outflow. Pressor doses further increased sodium excretion, indicating the presence of pressure natriuresis at these high doses.Keywords: renal haemodynamics, kidney function, natriuresis, dopamine, dose-response, tubular function, lithium clearance, sodium hydronephrotic kidney of the rat [4], thus supporting the Introduction concept of a vasodilating effect of specific dopaminergic D 1 -receptor activation, which at higher doses is opposed by In anaesthetized dogs [1] and rats [2], low doses of dopamine decreased renal vascular resistance, whereas higher doses an action of a-adrenergic receptors [5,6]. Another important effect of dopamine, which does not occur with other caused vasoconstriction.…”

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confidence: 82%

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Dopamine natriuresis in salt-repleted, water-loaded humans: a dose-response study

Olsen¹,

Olsen

Bonde³

et al. 1997

Br J Clin Pharmacol

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AimsThe purpose of the present study was to define the dose-response relationship between exogenous dopamine and systemic haemodynamics, renal haemodynamics, and renal excretory function at infusion rates in the range 0 to 12.5 mg kg −1 min −1 in normal volunteers. Methods While undergoing water diuresis, eight subjects were infused with 0, 1, 2, 3, 5, 7.5, 10 or 12.5 mg of dopamine kg −1 min −1 over 2 h in a randomized and double-blind fashion. On each study day, renal clearance studies were performed during a 1 h baseline period and subsequently during the second 1 h infusion period. Lithium clearance (CL Li ) was used to estimate proximal tubular outflow.Results Cardiac output increased with the four highest doses. Mean arterial pressure followed a biphasic pattern with a decrease during the two lowest doses and a dosedependent increase from the 7.5 mg kg Conclusions In conclusion, the renal vasodilating effect of dopamine was maximal with 3 mg kg −1 min −1 . The dose-dependent attenuation seen with higher doses is consistent with an increased a-adrenergic stimulation opposing the effect on dopaminergic receptors. The present CL Li studies confirm that dopamine increases proximal tubular outflow. The results suggest that the natriuretic effect of depressor doses of dopamine was primarily caused by attenuation of the increase in distal sodium reabsorption normally seen after an increase in proximal tubular outflow. Pressor doses further increased sodium excretion, indicating the presence of pressure natriuresis at these high doses.Keywords: renal haemodynamics, kidney function, natriuresis, dopamine, dose-response, tubular function, lithium clearance, sodium hydronephrotic kidney of the rat [4], thus supporting the Introduction concept of a vasodilating effect of specific dopaminergic D 1 -receptor activation, which at higher doses is opposed by In anaesthetized dogs [1] and rats [2], low doses of dopamine decreased renal vascular resistance, whereas higher doses an action of a-adrenergic receptors [5,6]. Another important effect of dopamine, which does not occur with other caused vasoconstriction. a-adrenergic receptor blockade abolished the vasoconstriction so that vasodilation was catecholamines, is the increase in sodium excretion [5][6][7]. Stimulation of D 1 -receptors in proximal tubular brushobserved with all doses of dopamine [2]. These dosedependent effects have been confirmed in studies using border membranes inhibits the Na

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“…By counteracting a dopamine-dependent vasodilatation, and consequently increasing the cortico-medullary osmotic gradient, dopamine antagonists could favour collecting tubule water reabsorption (Chapman et al, 1980). This would mimic the effect ofenhanced plasma ADH concentration and lead to reduced urine flow and increased urine osmolality.…”

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confidence: 99%

Effect of dopamine antagonists on the urine flow of rats infused with hypotonic saline

Angchanpen

Marin-Grez

Schnermann

1988

British J Pharmacology

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1 The probable involvement of dopamine in the regulation of water excretion was investigated by administering dopamine antagonists intravenously to barbiturate -anaesthetized rats undergoing a water diuresis induced by the infusion of 0.83% glucose with 0.3% NaCl at the rate of 9 ml h-'. 2 Administration of 100l ig of the D,-/D2-dopamine antagonist, haloperidol, reduced the enhanced urine flow of rats infused with the hypotonic solution by 69% (from 75.4 ± 13.0 to 23.6 ± 6.0 pI min-', P<0.01). Similarly, the D,-receptor antagonist, SCH23390, reduced urine flow by 58% (from 77.5 ± 9.2 to 32.7 ± 7.2p fmin-', P <0.01) and the D2-receptor antagonist, sulpiride, by 47% (from 66.2 ± 8.6 to 35.1 ± 6.8 pidmin-', P < 0.05).3 The injection of SCH 23390 increased the urine osmolality from 189.6 ± 27.5 to 479.8 ± 45.8 mosm kg-' (P < 0.05). There was no significant change in sodium and potassium excretion in any of the experiments. Blood pressure (BP) decreased after haloperidol and SCH 23390 injection from control values of 121.7 ± 1.7 and 116.5 ± 7.4 to 113.3 ± 3.3 and 106.0 ± 8.8 mmHg respectively (P < 0.05). 4 To study whether the influence of dopamine antagonists on urine flow during water diuresis depends on antidiuretic hormone (ADH), we administered 0.6 Ag d(CH2)5-D-Phe-Ile-AVP (an ADH antagonist) shortly after the injection of l00 g SCH 23390. The preferential V2 ADH-antagonist abolished the antidiuretic effect of SCH 23390 but did not affect its blood pressure reducing effect (from 118.6 ± 5.6 to 103.2 ± 4.6 mmHg, P <0.01). 5 These results suggest that dopamine antagonists blunted the hypotonic saline-induced diuresis by favouring ADH release through an interference with an inhibitory dopaminergic pathway.

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The actions of dopamine and of sulpiride on regional blood flows in the rat kidney.

Cited by 62 publications

References 15 publications

Dopamine- and cAMP-regulated phosphoprotein (DARPP-32) and dopamine DA1 agonist-sensitive Na+,K+-ATPase in renal tubule cells.

Dopamine- and cAMP-regulated phosphoprotein (DARPP-32) and dopamine DA1 agonist-sensitive Na+,K+-ATPase in renal tubule cells.

Dopamine natriuresis in salt-repleted, water-loaded humans: a dose-response study

Effect of dopamine antagonists on the urine flow of rats infused with hypotonic saline

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