Na+/H+ exchange activity and NHE-3 expression in renal tubules from the spontaneously hypertensive rat

LaPointe, Michael S.; Sodhi, Chhinder P.; Sahai, Atul; Batlle, Daniel

doi:10.1046/j.1523-1755.2002.00406.x

Cited by 56 publications

(57 citation statements)

References 39 publications

(7 reference statements)

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“…Previous studies have shown that sodium reabsorption in the proximal tubule is also increased in the SHR (Biollaz et al, 1986;Firth et al, 1989). Studies also show that sodium transporters of the proximal tubule, namely the NHE-3 and Na ϩ -K ϩ -ATPase, are up-regulated in the SHR kidney (Tsuruya et al, 1991;LaPointe et al, 2002). Our data are in concordance with these findings.…”

Section: Increased Expression Of Bsc-1 In Shr 1057supporting

confidence: 93%

“…at ASPET Journals on May 11, 2018 jpet.aspetjournals.org sponsible for the increase in protein expression and activity of the NHE-3 transporter as well as Na ϩ -K ϩ -ATPase in the SHR (Hayward et al, 1999;LaPointe et al, 2002). Whether higher steady-state levels of BSC-1, ROMK-1, and AQP-1 in SHR are due to greater translational efficiency or enhanced stability of the proteins or both cannot be deduced from the present study.…”

Section: Increased Expression Of Bsc-1 In Shr 1057mentioning

confidence: 60%

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Increased Expression of the Sodium Transporter BSC-1 in Spontaneously Hypertensive Rats

Sonalker

Tofovic²,

Jackson³

2004

J Pharmacol Exp Ther

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The purpose of this study was to compare the expression of BSC-1 (bumetanide-sensitive Na ϩ -K ϩ -2Cl Ϫ cotransporter) in kidneys of spontaneously hypertensive rats (SHR) versus Wistar-Kyoto (WKY) rats by immunoblotting and reverse transcription-polymerase chain reaction. To determine the specificity of any observed changes in BSC-1 expression, we also compared expression of the thiazide sensitive Na ϩ -Cl Ϫ cotransporter (TSC), the type-3 Na ϩ -H ϩ exchanger (NHE-3), Na ϩ -K ϩ -ATPase-␣ 1 , the inwardly rectifying K ϩ channel (ROMK-1), the type-1 Na ϩ -HCO 3 Ϫ cotransporter (NBC-1), aquaporin-1, and aquaporin-2. Analyses were performed on outer cortex, outer medulla, and inner medulla. BSC-1 protein was detected in outer medulla and was markedly (6-fold) higher in SHR. TSC protein was detected in the cortex and was not overexpressed in SHR. Aquaporin-1 protein was detected in all three regions and was not overexpressed in SHR. Aquaporin-2 and ROMK-1 proteins were detected in all three regions, but were moderately elevated (2-fold) only in the SHR inner medulla. Na ϩ -K ϩ -ATPase and NHE-3 proteins were detected in all three regions. Na ϩ -K ϩ -ATPase-␣ 1 was modestly (25%) increased in SHR outer and inner medulla, whereas NHE-3 was moderately (2-fold) increased in the SHR cortex and inner medulla. NBC-1 protein was detected only in the cortex and was higher (2-fold) in SHR. mRNA levels of BSC-1, aquaporin-2, and ROMK-1 were not elevated in SHR, indicating a post-translational mechanism of protein overexpression. High-dose furosemide increased fractional sodium excretion more in SHR than WKY (3-fold). We conclude that increased expression of BSC-1, and to a lesser extent, aquaporin-2, ROMK-1, NHE-3, and NBC-1 may contribute to the pathogenesis of hypertension in the SHR.

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Section: Increased Expression Of Bsc-1 In Shr 1057supporting

confidence: 93%

Section: Increased Expression Of Bsc-1 In Shr 1057mentioning

confidence: 60%

Increased Expression of the Sodium Transporter BSC-1 in Spontaneously Hypertensive Rats

Sonalker

Tofovic²,

Jackson³

2004

J Pharmacol Exp Ther

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“…However, in the young (5 weeks), basal proximal tubular reabsorption is greater in the SHR than in the WKY rat which was shown to be due to increased basal angiotensin II effect [14], and NHE3 activity is increased especially at 6 weeks of age: expression may or may not be increased [15][16][17][18]. These studies support our findings of increased Cl -/HCO 3 -and NHE3 activity as the renal proximal tubule cells were obtained from 4-8 weeks old rats [19].…”

Section: Introductionmentioning

confidence: 99%

Increased responsiveness to JNK1/2 mediates the enhanced H2O2-induced stimulation of Cl−/HCO3− exchanger activity in immortalized renal proximal tubular epithelial cells from the SHR

Simão¹,

Gomes²,

José³

et al. 2010

Biochemical Pharmacology

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. Increased responsiveness to JNK1/2 mediates the enhanced HO-induced stimulation of Cl/HCO exchanger activity in immortalized renal proximal tubular epithelial cells from the SHR. Biochemical Pharmacology, Elsevier, 2010, 80 (6) This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

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“…Given the important role of NHE3 in mediating sodium and fluid reabsorption, this transporter is subject to acute and chronic regulation in response to a variety of conditions affecting salt balance, including volume contraction (9), high salt intake (33,45), and hypertension (16,21,25,46). Using an experimental animal model of chronic volume contraction, Fisher et al (9) observed that NHE3 expression is significantly upregulated in the renal cortex at both protein and mRNA levels.…”

mentioning

confidence: 99%

Posttranslational mechanisms associated with reduced NHE3 activity in adult vs. young prehypertensive SHR

Crajoinas

Lessa

Carraro‐Lacroix

et al. 2010

American Journal of Physiology-Renal Physiology

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Abnormalities in renal proximal tubular (PT) sodium transport play an important role in the pathophysiology of essential hypertension. The Na+/H+ exchanger isoform 3 (NHE3) represents the major route for sodium entry across the apical membrane of renal PT cells. We therefore aimed to assess in vivo NHE3 transport activity and to define the molecular mechanisms underlying NHE3 regulation before and after development of hypertension in the spontaneously hypertensive rat (SHR). NHE3 function was measured as the rate of bicarbonate reabsorption by means of in vivo stationary microperfusion in PT from young prehypertensive SHR (Y-SHR; 5-wk-old), adult SHR (A-SHR; 14-wk-old), and age-matched Wistar Kyoto (WKY) rats. We found that NHE3-mediated PT bicarbonate reabsorption was reduced with age in the SHR (1.08 ± 0.10 vs. 0.41 ± 0.04 nmol/cm2×s), while it was increased in the transition from youth to adulthood in the WKY rat (0.59 ± 0.05 vs. 1.26 ± 0.11 nmol/cm2×s). Higher NHE3 activity in the Y-SHR compared with A-SHR was associated with a predominant microvilli confinement and a lower ratio of phosphorylated NHE3 at serine-552 to total NHE3 (P-NHE3/total). After development of hypertension, P-NHE3/total increased and NHE3 was retracted out of the microvillar microdomain along with the regulator dipeptidyl peptidase IV (DPPIV). Collectively, our data suggest that the PT is playing a role in adapting to the hypertension in the SHR. The molecular mechanisms of this adaptation possibly include an increase of P-NHE3/total and a redistribution of the NHE3-DPPIV complex from the body to the base of the PT microvilli, both predicted to decrease sodium reabsorption.

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Na+/H+ exchange activity and NHE-3 expression in renal tubules from the spontaneously hypertensive rat

Cited by 56 publications

References 39 publications

Increased Expression of the Sodium Transporter BSC-1 in Spontaneously Hypertensive Rats

Increased Expression of the Sodium Transporter BSC-1 in Spontaneously Hypertensive Rats

Increased responsiveness to JNK1/2 mediates the enhanced H2O2-induced stimulation of Cl−/HCO3− exchanger activity in immortalized renal proximal tubular epithelial cells from the SHR

Posttranslational mechanisms associated with reduced NHE3 activity in adult vs. young prehypertensive SHR

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