Atrial natriuretic peptide inhibits amiloride-sensitive sodium uptake in rat brain

Kanda, F. A.; Sarnacki, P.; Arieff, Allen I.

doi:10.1152/ajpregu.1992.263.2.r279

Cited by 10 publications

(10 citation statements)

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“…ANP can early regulate pHi through NHE-1 [12,13,34]. In fact, pharmacological concentrations of the hormone inhibit NHE-1 by a mechanism that includes increased intracellular levels of cGMP, while physiological concentrations can stimulate NHE-1 through the diacylglycerol production or cAMP decrease [13].…”

Section: Discussionmentioning

confidence: 99%

“…Among different biological effects, in hepatoblastoma (HepG2) cells, ANP inhibits cell proliferation through the selective upregulation of the expression of the NPR-C receptors associated with decreased intracellular concentrations of cAMP [11]. Furthermore, ANP can inhibit or stimulate Na + /H + exchanger isoform 1 (NHE-1) depending on cell type [12,13].…”

Section: Introductionmentioning

confidence: 99%

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Atrial Natriuretic Peptide Effects on Intracellular pH Changes and ROS Production in HEPG2 Cells: Role of p38 MAPK and Phospholipase D

Baldini¹,

Vito²,

Vismara³

et al. 2005

Cell Physiol Biochem

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Aims: The present study was performed to evaluate Atrial Natriuretic Peptide (ANP) effects on intracellular pH, phospholipase D and ROS production and the possible relationship among them in HepG2 cells. Cancer extracellular microenvironment is more acidic than normal tissues and the activation of NHE-1, the only system able to regulate pHi homeostasis in this condition , can represent an important event in cell proliferation and malignant transformation. Methods: The ANP effects on pHi were evaluated by fluorescence spectrometry. The effects on p38 MAPK and ROS production were evaluated by immunoblots and analysis of DCF-DA fluorescence, respectively. RT-PCR analysis and Western blotting were used to determine the ANP effect on mRNA NHE-1 expression and protein levels. PLD-catalyzed conversion of phosphatidylcholine to phosphatydilethanol (PetOH), in the presence of ethanol, was monitored by thin layer chromatography. Results: A significant pHi decrease was observed in ANP-treated HepG2 cells and this effect was paralleled by the enhancement of PLD activity and ROS production. The ANP effect on pHi was coupled to an increased p38 MAPK phosphorylation and a down-regulation of mRNA NHE-1 expression and protein levels. Moreover, the relationship between PLD and ROS production was demonstrated by calphostin-c, a potent inhibitor of PLD. At the same time, all assessed ANP-effects were mediated by NPR-C receptors. Conclusion: Our results indicate that ANP recruits a signal pathway associated with p38 MAPK, NHE-1 and PLD responsible for ROS production, suggesting a possible role for ANP as novel modulator of ROS generation in HepG2 cells.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Atrial Natriuretic Peptide Effects on Intracellular pH Changes and ROS Production in HEPG2 Cells: Role of p38 MAPK and Phospholipase D

Baldini¹,

Vito²,

Vismara³

et al. 2005

Cell Physiol Biochem

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“…Amiloride-sensitive sodium uptake. Sodium uptake was determined in synaptosomes with or without amiloride (1 mM) (25). An aliquot of synaptosomes was incubated with four volumes ofpreequilibrium media ([in mM] KCl, 150; MgCl2, 1; Hepes-Tris, 5; pH 7.40) for 10 min at 37°C.…”

Section: Methodsmentioning

confidence: 99%

Hypoxic and ischemic hypoxia exacerbate brain injury associated with metabolic encephalopathy in laboratory animals.

Vexler

Ayus²,

Roberts³

et al. 1994

J. Clin. Invest.

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Hypoxemia is a major comorbid factor for permanent brain damage in several metabolic encephalopathies. To determine whether hypoxia impairs brain adaptation to hyponatremia, worsening brain edema, we performed in vitro and in vivo studies in cats and rats with hyponatremia plus either ischemic or hypoxic hypoxia. Mortality with hypoxic hypoxia was 0%; with hyponatremia, 22%; and with hyponatremia + hypoxia, 100%. Hyponatremia in cats produced brain edema, with a compensatory decrease of brain sodium. Ischemic hypoxia also resulted in brain edema, but with elevation of brain sodium. However, when ischemic hypoxia was superimposed upon hyponatremia, there was elevation of brain sodium with further elevation of water. Outward sodium transport in cat cerebral cortex synaptosomes was measured via three major pathways through which brain osmolality can be decreased. After hyponatremia, sodium transport was significantly altered such that brain cell osmolality would decrease: 44% increase in Na+-K+-ATPase transport activity (ouabain inhibitable); 26% decrease in amiloride-sensitive sodium uptake. The change in veratridine-stimulated sodium uptake was not significant (P > 0.05). When ischemic hypoxia was superimposed upon hyponatremia, all of the cerebral adaptive changes induced by hyponatremia alone were eliminated. Thus, hypoxia combined with hyponatremia produces a major increase in brain edema and mortality, probably by eliminating the compensatory mechanisms of sodium transport initiated by hyponatremia that tend to minimize brain swelling. (J. Clin. Invest. 1994.93:256-264.)

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“…More than fifteen years ago, it has been reported that ANP is able to modify the intracellular pH by inhibiting or stimulating the NHE-1, depending on the cell type [55, 56]. In the 2005, Baldini and collaborators demonstrated that in HepG2 hepatoblastoma cells, ANP induced intracellular acidification by decreasing NHE-1 expression and activity [57].…”

Section: Innovative Targets For Antitumor Activity Of Anpmentioning

confidence: 99%

Atrial Natriuretic Peptide: A Magic Bullet for Cancer Therapy Targeting Wnt Signaling and Cellular pH Regulators

Serafino¹,

Pierimarchi

2014

CMC

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Atrial natriuretic peptide (ANP) is a cardiac hormone playing a crucial role in cardiovascular homeostasis mainly through blood volume and pressure regulation. In the last years, the new property ascribed to ANP of inhibiting tumor growth both in vitro and in vivo has made this peptide an attractive candidate for anticancer therapy. The molecular mechanism underlying the anti-proliferative effect of ANP has been mainly related to its interaction with the specific receptors NPRs, through which this natriuretic hormone inhibits some metabolic targets critical for cancer development, including the Ras-MEK1⁄2-ERK1⁄2 kinase cascade, functioning as a multikinase inhibitor. In this review we summarize the current knowledge on this topic, focusing on our recent data demonstrating that the antitumor activity of this natriuretic hormone is also mediated by a concomitant effect on the Wnt/β-catenin pathway and on the pH regulation ability of cancer cells, through a Frizzled-related mechanism. This peculiarity of simultaneously targeting two processes crucial for neoplastic transformation and solid tumor survival reinforces the utility of ANP for the development of both preventive and therapeutic strategies.

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Atrial natriuretic peptide inhibits amiloride-sensitive sodium uptake in rat brain

Cited by 10 publications

References 0 publications

Atrial Natriuretic Peptide Effects on Intracellular pH Changes and ROS Production in HEPG2 Cells: Role of p38 MAPK and Phospholipase D

Atrial Natriuretic Peptide Effects on Intracellular pH Changes and ROS Production in HEPG2 Cells: Role of p38 MAPK and Phospholipase D

Hypoxic and ischemic hypoxia exacerbate brain injury associated with metabolic encephalopathy in laboratory animals.

Atrial Natriuretic Peptide: A Magic Bullet for Cancer Therapy Targeting Wnt Signaling and Cellular pH Regulators

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