Renal Dopamine System

Carey, Robert M.

doi:10.1161/hy0901.096422

Cited by 132 publications

(54 citation statements)

References 71 publications

(68 reference statements)

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“…Little is known about the mechanisms by which DA is stored in proximal tubule cells [28]. Renal DA availability can be regulated at different metabolic levels such as synthesis, storage or catabolism [29].…”

Section: Discussionmentioning

confidence: 99%

Angiotensin II Regulates Extraneuronal Dopamine Uptake in the Kidney

Choi

Correa²,

Turco³

et al. 2006

Nephron Physiol

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Background/Aims: Angiotensin II (ANG II) and dopamine (DA) are both important regulators of sodium and water transport across renal proximal tubules. Previous studies demonstrate that atrial natriuretic factor (ANF) can regulate renal DA uptake and thereby Na⁺,K⁺-ATPase activity in the external renal cortex. As ANG II counteracts most of the ANF biological effects, the aim of the present study was to evaluate ANG II effects on renal DA metabolism and identify the receptor involved. Methods: To determine ANG II effects on renal DA metabolism, we evaluated ³H-DA uptake in vitro in kidney tissue samples from Sprague-Dawley rats. Results: The results indicate that ANG II decreased DA uptake at 30 min, in a concentration-response fashion, in the external and juxtamedullar cortex. DA uptake was characterized as an extraneuronal uptake and decreased at 0°C and in sodium-free medium. The biological receptor type involved was AT₁, since losartan reversed ANG II effects on DA uptake while AT₂ receptors were not involved since PD 123319 did not affect ANG II effects. The absence of sodium did not alter the ANG II response. Conclusion: ANG II inhibits DA uptake by kidney tubular cells. These effects implicate AT₁ receptors without participation of AT₂ receptors. This mechanism could be related to the DA effects on sodium reabsorption and linked to ANG II antinatriuretic effects in the kidney.

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Section: Discussionmentioning

confidence: 99%

Angiotensin II Regulates Extraneuronal Dopamine Uptake in the Kidney

Choi

Correa²,

Turco³

et al. 2006

Nephron Physiol

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“…Dopamine is the most important natriuretic signal to the proximal tubule [2, 11]. Urinary dopamine derives largely from circulating L-DOPA [4, 6], and proximal tubules are a source for this excreted dopamine [5].…”

Section: Regulation Of Flow-activated Proximal Tubule Function By Secmentioning

confidence: 99%

Regulation of glomerulotubular balance: flow-activated proximal tubule function

Wang

Weinbaum

Weinstein

2017

Pflugers Arch - Eur J Physiol

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The purpose of this review is to summarize our knowledge and understanding of the physiological importance and the mechanisms underlying flow-activated proximal tubule transport. Since the earliest micropuncture studies of mammalian proximal tubule, it has been recognized that tubular flow is an important regulator of sodium, potassium, and acid-base transport in the kidney. Increased fluid flow stimulates Na+ and HCO3− absorption in the proximal tubule via stimulation of Na/H-exchanger isoform 3 (NHE3) and H+-ATPase. In the proximal tubule, brush border microvilli are the major flow sensors, which experience changes in hydrodynamic drag and bending moment as luminal flow velocity changes and which transmit the force of altered flow to cytoskeletal structures within the cell. The signal to NHE3 depends upon the integrity of the actin cytoskeleton; the signal to the H+-ATPase depends upon microtubules. We have demonstrated that alterations in fluid drag impact tubule function by modulating ion transporter availability within the brush border membrane of the proximal tubule. Beyond that, there is evidence that transporter activity within the peritubular membrane is also modulated by luminal flow. Secondary messengers that regulate the flow-mediated tubule function have also been delineated. Dopamine blunts the responsiveness of proximal tubule transporters to changes in luminal flow velocity, while a DA1 antagonist increases flow sensitivity of solute reabsorption. IP3 receptor-mediated intracellular Ca2+ signaling is critical to transduction of microvillus drag. In this review, we summarize our findings of the regulatory mechanism of flow-mediated Na+ and HCO3− transport in the proximal tubule and review available information about flow sensing and regulatory mechanism of glomerulotubular balance.

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“…The process that determines the balance of hormonal action, and how DA can reduce proximal tubule Na ϩ reabsorption in the presence of saturating concentrations of the antagonistic Ang II, are some of the mechanistic aspects that remain to be elucidated. Although some insights regarding the regulation by DA have been reported by us and other researchers, the molecular mechanism by which Ang II regulates the activity of the proteins involved in proximal tubule Na ϩ reabsorption is still unknown (10,11,(15)(16)(17)(18). In this study, we have investigated the cellular mechanisms beyond the antagonistic actions of Ang II and DA and how these mechanisms are dependent on changes in intracellular Na ϩ concentration.…”

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confidence: 94%

Intracellular Na+ Regulates Dopamine and Angiotensin II Receptors Availability at the Plasma Membrane and Their Cellular Responses in Renal Epithelia

Efendiev

Budu

Cinelli

et al. 2003

Journal of Biological Chemistry

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The balance and cross-talk between natruretic and antinatruretic hormone receptors plays a critical role in the regulation of renal Na ؉ homeostasis, which is a major determinant of blood pressure. Dopamine and angiotensin II have antagonistic effects on renal Na ؉ and water excretion, which involves regulation of the Na ؉ ,K ؉ -ATPase activity. Herein we demonstrate that angiotensin II (Ang II) stimulation of AT1 receptors in proximal tubule cells induces the recruitment of Na ؉ ,K ؉ -ATPase molecules to the plasmalemma, in a process mediated by protein kinase C␤ and interaction of the Na ؉ ,K ؉ -ATPase with adaptor protein 1. Ang II stimulation led to phosphorylation of the ␣ subunit Ser-11 and Ser-18 residues, and substitution of these amino acids with alanine residues completely abolished the Ang II-induced stimulation of Na ؉ ,K ؉ -ATPase-mediated Rb ؉ transport. Thus, for Ang II-dependent stimulation of Na ؉ ,K ؉ -ATPase activity, phosphorylation of these serine residues is essential and may constitute a triggering signal for recruitment of Na ؉ ,K ؉ -ATPase molecules to the plasma membrane. When cells were treated simultaneously with saturating concentrations of dopamine and Ang II, either activation or inhibition of the Na ؉ ,K ؉ -ATPase activity was produced dependent on the intracellular Na ؉ concentration, which was varied in a very narrow physiological range (9 -19 mM). A small increase in intracellular Na ؉ concentrations induces the recruitment of D1 receptors to the plasma membrane and a reduction in plasma membrane AT1 receptors. Thus, one or more proteins may act as an intracellular Na ؉ concentration sensor and play a major regulatory role on the effect of hormones that regulate proximal tubule Na ؉ reabsorption.

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Renal Dopamine System

Cited by 132 publications

References 71 publications

Angiotensin II Regulates Extraneuronal Dopamine Uptake in the Kidney

Angiotensin II Regulates Extraneuronal Dopamine Uptake in the Kidney

Regulation of glomerulotubular balance: flow-activated proximal tubule function

Intracellular Na+ Regulates Dopamine and Angiotensin II Receptors Availability at the Plasma Membrane and Their Cellular Responses in Renal Epithelia

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