Increases in transepithelial vectorial Na+ transport facilitates Na+-dependent l-DOPA transport in renal OK cells

Silva, E.; Gomes, Pedro; Soares-da-Silva, Patrı́cio

doi:10.1016/j.lfs.2006.02.018

Cited by 9 publications

(11 citation statements)

References 40 publications

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“…To address a possible regulatory role by ␣ 2C -adrenoceptors on L-DOPA uptake in the kidney, we began by evaluating the effect of receptor activation on L-DOPA uptake in a cellular model of proximal tubule cells: OK cells. These cells have long been used to characterize the mechanisms of L-DOPA transport (18,44,59), and what is more, a study (5) of the expression of adrenoceptors in these cells has shown that the ␣ 2C -subtype is the only ␣ 2 -adrenoceptor present. The data presented here show that the activation of ␣ 2C -adrenoceptors by medetomidine produced a concentration-dependent decrease in the uptake of L-DOPA and that this effect was abolished by the presence of the selective ␣ 2C -adrenoceptor antagonist JP-1302.…”

Section: Discussionmentioning

confidence: 99%

“…Studies have shown that different subclonal lines (19,44) or serial passaging (46,47) are associated with differences in cell structure that result in differences in L-amino acid transporter activity (37) and in signaling activity (45). Although the characteristics of the transporter involved in L-DOPA uptake in OK cells of the clonal line and the passage number used in this study have been reported to be those of LAT1 (18), given this may be subject to variability, we have sought to characterize the transporter involved in L-DOPA uptake.…”

Section: Discussionmentioning

confidence: 99%

“…The candidate transport systems for L-DOPA include the Na ϩ -dependent systems B 0 , B 0,ϩ and y ϩ L and the Na ϩ -independent systems L-amino acid transporters (LAT1 and LAT2) and b 0,ϩ (18 -19, 38, 49). Opossum kidney (OK) cells are an established epithelial cell line that has been used for the study of L-DOPA transport (18,44,59). In OK cells, although LAT1 and LAT2 as well as system ASC amino acid transporter-2 (ASCT2) have been identified and shown to play a role in the uptake of amino acids (37), L-DOPA uptake in this cell line proceeds through LAT1 (18).…”

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confidence: 99%

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α_2C-Adrenoceptors modulatel-DOPA uptake in opossum kidney cells and in the mouse kidney

Moura

Silva

Serrão

et al. 2012

American Journal of Physiology-Renal Physiology

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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α_2C-Adrenoceptors modulatel-DOPA uptake in opossum kidney cells and in the mouse kidney

Moura

Silva

Serrão

et al. 2012

American Journal of Physiology-Renal Physiology

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“…Considering the huge availability of aromatic amino acid decarboxylase in the proximal tubule, it has been proposed that the rate-limiting step in the synthesis of dopamine in the renal tubules is the uptake of L-dopa (3,21). A variety of sodium-dependent amino acid transporters have been implicated in the uptake of L-dopa by proximal tubule cells (29,34). In a recent publication, Pinho et al (27) demonstrated a parallelism between the expression of sodium-dependent neutral amino acid transporters ASCT2 and B(0)AT1, the uptake of L-dopa by isolated renal tubules, and the excretion of urinary dopamine in spontaneously hypertensive rats on a high-salt intake.…”

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confidence: 99%

Signaling cascade of insulin-induced stimulation of l-dopa uptake in renal proximal tubule cells

Carranza¹,

Musolino²,

Villar³

et al. 2008

American Journal of Physiology-Cell Physiology

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The inward l-dihydroxyphenylalanine (L-dopa) transport supplies renal proximal tubule cells (PTCs) with the precursor for dopamine synthesis. We have previously described insulin-induced stimulation of L-dopa uptake into PTCs. In the present paper we examined insulin-related signaling pathways involved in the increase of l-dopa transport into isolated rat PTCs. Insulin (50-500 microU/ml) increased L-dopa uptake by PTCs, reaching the maximal increment (60% over the control) at 200 microU/ml. At this concentration, insulin also increased insulin receptor tyrosine phosphorylation. Both effects were abrogated by the tyrosine kinase inhibitor genistein (5 microM). In line, inhibition of the protein tyrosine phosphatase by pervanadate (0.2-100 microM) caused a concentration-dependent increase in both the uptake of L-dopa (up to 400%) and protein tyrosine phosphorylation. A synergistic effect between pervanadate and insulin on L-dopa uptake was observed only when threshold (0.2 microM), but not maximal (5 microM), concentrations of pervanadate were assayed. Insulin-induced stimulation of L-dopa uptake was also abolished by inhibition of phosphatidylinositol 3-kinase (PI3K; 100 nM wortmannin, and 25 microM LY-294002) and protein kinase C (PKC; 1 microM RO-318220). Insulin-induced activation of PKC-zeta was confirmed in vitro by its translocation from the cytosol to the membrane fraction, and in vivo by immunohistochemistry studies. Insulin caused a wortmannin-sensitive increase in Akt/protein kinase B (Akt/PKB) phosphorylation and a dose-dependent translocation of Akt/PKB to the membrane fraction. Our findings suggest that insulin activates PKC-zeta, and Akt/PKB downstream of PI3K, and that these pathways contribute to the insulin-induced increase of L-dopa uptake into PTCs.

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“…The conversion of L-Dopa into dopamine in the kidneys provides virtually all the free urinary dopamine [19]. L-Dopa uptake by the proximal tubule cells is stimulated by Na + -independent and Na + -dependent transporters through the apical membrane [20]. The inward Na + gradient apparently stimulates the apical Na + -dependent L-Dopa influx via a Na + -dependent L-Dopa transporter, namely, amino acid transport system B 0 (system B 0 ) [20–24].…”

Section: Renal Dopamine: Function and Regulation Steps Of A Local mentioning

confidence: 99%

Atrial Natriuretic Peptide and Renal Dopaminergic System: A Positive Friendly Relationship?

Choi

Mikusic

Kouyoumdzian

et al. 2014

BioMed Research International

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Sodium metabolism by the kidney is accomplished by an intricate interaction between signals from extrarenal and intrarenal sources and between antinatriuretic and natriuretic factors. Renal dopamine plays a central role in this interactive network. The natriuretic hormones, such as the atrial natriuretic peptide, mediate some of their effects by affecting the renal dopaminergic system. Renal dopaminergic tonus can be modulated at different steps of dopamine metabolism (synthesis, uptake, release, catabolism, and receptor sensitization) which can be regulated by the atrial natriuretic peptide. At tubular level, dopamine and atrial natriuretic peptide act together in a concerted manner to promote sodium excretion, especially through the overinhibition of Na+, K+-ATPase activity. In this way, different pathological scenarios where renal sodium excretion is dysregulated, as in nephrotic syndrome or hypertension, are associated with impaired action of renal dopamine and/or atrial natriuretic peptide, or as a result of impaired interaction between these two natriuretic systems. The aim of this review is to update and comment on the most recent evidences demonstrating how the renal dopaminergic system interacts with atrial natriuretic peptide to control renal physiology and blood pressure through different regulatory pathways.

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Increases in transepithelial vectorial Na+ transport facilitates Na+-dependent l-DOPA transport in renal OK cells

Cited by 9 publications

References 40 publications

α_2C-Adrenoceptors modulatel-DOPA uptake in opossum kidney cells and in the mouse kidney

α_2C-Adrenoceptors modulatel-DOPA uptake in opossum kidney cells and in the mouse kidney

Signaling cascade of insulin-induced stimulation of l-dopa uptake in renal proximal tubule cells

Atrial Natriuretic Peptide and Renal Dopaminergic System: A Positive Friendly Relationship?

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Increases in transepithelial vectorial Na+ transport facilitates Na+-dependent l-DOPA transport in renal OK cells

Cited by 9 publications

References 40 publications

α2C-Adrenoceptors modulatel-DOPA uptake in opossum kidney cells and in the mouse kidney

α2C-Adrenoceptors modulatel-DOPA uptake in opossum kidney cells and in the mouse kidney

Signaling cascade of insulin-induced stimulation of l-dopa uptake in renal proximal tubule cells

Atrial Natriuretic Peptide and Renal Dopaminergic System: A Positive Friendly Relationship?

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Product

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α_2C-Adrenoceptors modulatel-DOPA uptake in opossum kidney cells and in the mouse kidney

α_2C-Adrenoceptors modulatel-DOPA uptake in opossum kidney cells and in the mouse kidney