Urodilatin and dopamine: A new interaction in the kidney

Citarella, Marisa R.; Choi, Marcelo Roberto; Gironacci, Mariela M.; Medici, Cecilia; Correa, Alicia H.; Fernández, Belisario E.

doi:10.1016/j.regpep.2008.11.009

Cited by 20 publications

(23 citation statements)

References 37 publications

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“…Interstitial infusion of fenoldopam, a D1-like specific agonist, caused a proximal tubule-dependent natriuresis in salt-loaded adult rats [65], and coinfusion of an AT2 receptor-specific blocking compound, PD-123319 [66], blocked the effect, suggesting that the AT2 receptor is necessary for the full expression of the effect of D1 receptor activation in promoting sodium excretion. Other natriuretic factors (ANP/ANPA, eicosanoids, nitric oxide, urodilatin) also regulate D1-like receptor function [67][68][69][70]. It is likely that D1-like receptor may play a central role in the natriuretic effects of these factors, as has been shown for prolactin [53].…”

Section: Regulation Of D1-like Receptor Functionmentioning

confidence: 96%

Potential Dopamine-1 Receptor Stimulation in Hypertension Management

et al. 2011

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The role of dopamine receptors in blood pressure regulation is well established. Genetic ablation of both dopamine D1-like receptor subtypes (D1, D5) and D2-like receptor subtypes (D2, D3, D4) results in a hypertensive phenotype in mice. This review focuses on the dopamine D1-like receptor subtypes D1 and D5 (especially D1 receptors), as they play a major role in regulating sodium homeostasis and blood pressure. Studies mostly describing the role of renal dopamine D1-like receptors are included, as the kidneys play a pivotal role in the maintenance of sodium homeostasis and the long-term regulation of blood pressure. We also attempt to describe the interaction between D1-like receptors and other proteins, especially angiotensin II type 1 and type 2 receptors, which are involved in the maintenance of sodium homeostasis and blood pressure. Finally, we discuss a new concept of renal D1 receptor regulation in hypertension that involves oxidative stress mechanisms.

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Section: Regulation Of D1-like Receptor Functionmentioning

confidence: 96%

Potential Dopamine-1 Receptor Stimulation in Hypertension Management

et al. 2011

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“…Moreover, we have demonstrated that urodilatin, through stimulation of 3 H-dopamine uptake, favors dopamine intracellular accumulation, which in turn results in an over inhibition of renal Na + , K + -ATPase activity [4]. These previous findings lead us to hypothesize that urodilatin and the renal dopaminergic system could interact and enhance the natriuretic and diuretic effects of the peptide.…”

Section: Introductionmentioning

confidence: 80%

“…After preincubation, the tissues were transferred to 2.0 ml of fresh SKB medium and incubated for 30 min, in similar conditions, with 22.5 nM (0.625 μ Ci/ml)of 3 H-dopamine, 17 μM of nomifensine, without (control) or with the different tested drugs (experimental groups). We employed a concentration of 10 nM urodilatin according to the concentration-response curve obtained in previous experiments [4].…”

Section: Methodsmentioning

confidence: 99%

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Urodilatin increases renal dopamine uptake: intracellular network involved

et al. 2011

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Dopamine and urodilatin promote natriuresis and diuresis through a common pathway that involves reversible deactivation of renal Na+, K+-ATPase. We have reported that urodilatin enhances dopamine uptake in outer renal cortex through the natriuretic peptide type A receptor. Moreover, urodilatin enhances dopamine-induced inhibition of Na+, K+-ATPase activity. The objective of the present work was to investigate the intracellular signals involved in urodilatin effects on dopamine uptake in renal cortex of kidney rats. We show that urodilatin-elicited increase in ³H-dopamine was blunted by methylene blue (10 μM), a non-specific guanylate cyclase inhibitor, and by phorbol-12-myristate-13-acetate (1 μM), a particulate guanylate cyclase inhibitor, but not by 1H-[1,2,4]-oxadiazolo-[4,3-a]-quinoxalin-1-one (10 μM), a specific soluble guanylate cyclase inhibitor; therefore the involvement of particulate guanylate cyclase on urodilatin mediated dopamine uptake was confirmed. Cyclic guanosine monophosphate and proteinkinase G were also implicated in the signaling pathway, since urodilatin effects were mimicked by the analog 125 μM 8-Br-cGMP and blocked by the proteinkinase G-specific inhibitor, KT-5823 (1 μM). In conclusion, urodilatin increases dopamine uptake in renal cortex stimulating natriuretic peptide type A receptor, which signals through particulate guanylate cyclase activation, cyclic guanosine monophosphate generation, and proteinkinase G activation. Dopamine and urodilatin may achieve their effects through a common pathway that involves deactivation of renal Na+, K+-ATPase, reinforcing their natriuretic and diuretic properties.

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“…The synergism of DA and 20-hydroxyeicosatetraenoic acid, a major arachidonic acid metabolite of cytochrome P450, inhibits NKA activity in PCT via the D 1 signaling pathway (82). Urodilatin or DA decreases NKA activity, while urodilatin and DA combined, further decrease NKA activity, demonstrating an additive effect on the sodium pump, suggesting that urodilatin and DA act via a common intracellular pathway to decrease sodium and water tubular reabsorption, contributing to its natriuretic and diuretic effects (83). Additionally, synergistically interacting D 1 and NMDA receptors mediate non-vesicular transporter-depen- dent γ-aminobutyric acid (GABA) release in rat striatal medium spiny neurons through cAMP-dependent inhibition of NKA.…”

Section: Dicussion and Future Prospectsmentioning

confidence: 99%

Crosstalk between dopamine receptors and the Na+/K+-ATPase (Review)

Zhang

Liang³

et al. 2013

Molecular Medicine Reports

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Abstract. Dopamine (DA) receptors, which belong to the G protein-coupled receptor family, are the target of ~50% of all modern medicinal drugs and constitute a large and diverse class of proteins whose primary function is to transduce extracellular stimuli into intracellular signals. Na + /K + -ATPase (NKA) is ubiquitous and crucial for the maintenance of intracellular ion homeostasis and excitability. Furthermore, it plays a critical role in diverse effects, including clinical cardiotonic and cardioprotective effects, ischemic preconditioning in the brain, natriuresis, lung edema clearance and other processes. NKA regulation is of physiological and pharmacological importance and has species-and tissue-specific variations. The activation of DA receptors regulates NKA expression/activity and trafficking in various tissues and cells, for example in the kidney, lung, intestine, brain, non-pigmented ciliary epithelium and the vascular bed. DA receptor-mediated regulation of NKA mediates a diverse range of cellular responses and includes endocytosis/exocytosis, phosphorylation/dephosphorylation of the α subunit of NKA and multiple signaling pathways, including phosphatidylinositol (PI)-phospholipase C/protein kinase (PK) C, cAMP/PKA, PI3K, adaptor protein 2, tyrosine phosphatase and mitogen-activated protein kinase/extracellular signal-regulated protein kinase. Furthermore, in brain and HEK293T cells, D 1 and D 2 receptors exist in a complex with NKA. Among D 1 and D 2 receptors and NKA, regulations are reciprocal, which leads to crosstalk between DA receptors and NKA. In the present study, the current understanding of signaling mechanisms responsible for the crosstalk between DA receptors and NKA, as well as with specific consequent functions, is reviewed.

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Urodilatin and dopamine: A new interaction in the kidney

Cited by 20 publications

References 37 publications

Potential Dopamine-1 Receptor Stimulation in Hypertension Management

Potential Dopamine-1 Receptor Stimulation in Hypertension Management

Urodilatin increases renal dopamine uptake: intracellular network involved

Crosstalk between dopamine receptors and the Na+/K+-ATPase (Review)

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