scholarly journals Increased renal ENaC subunits and sodium retention in rats with chronic heart failure

2011 ◽  
Vol 300 (3) ◽  
pp. F641-F649 ◽  
Author(s):  
Hong Zheng ◽  
Xuefei Liu ◽  
U. S. Rao ◽  
Kaushik P. Patel
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Water Retention ◽  
Collecting Duct ◽  
Renal Nerves ◽  
Tubular Dysfunction ◽  
Renal Tubular Dysfunction ◽  
Sodium Retention ◽  
Coronary Ligation ◽  
Renal Tubular

Renal tubular dysfunction could be involved in the increased sodium and water reabsorption in chronic heart failure (CHF). The goal of the present study was to examine the molecular basis for the increased renal sodium and water retention in CHF. We hypothesized that dysregulation of renal epithelial sodium channels (ENaC) could be involved in the pathogenesis of CHF. The left coronary ligation-induced model of heart failure in the rat was used. Real-time PCR and Western blot analysis indicated that the mRNA and protein abundance of α-, β-, and γ-subunits of ENaC were significantly increased by in the cortex (mRNA: α-ENaC Δ104 ± 24%, β-ENaC Δ47 ± 16%, γ-ENaC Δ55 ± 18%; protein: α-ENaC Δ114 ± 28%, β-ENaC Δ150 ± 31%, γ-ENaC Δ39 ± 5% compared with sham rats) and outer medulla (mRNA: α-ENaC Δ52 ± 18%, β-ENaC Δ38 ± 8%, γ-ENaC Δ39 ± 13%; protein: α-ENaC Δ88 ± 16%, β-ENaC Δ94 ± 28%, γ-ENaC Δ45 ± 9% compared with sham rats) of CHF compared with sham-operated rats. Immunohistochemistry microscopy confirmed the increased labeling of α-, β-, and γ-ENaC subunits in the collecting duct segments in rats with CHF. Furthermore, there was a significant increase in diuretic (7-fold compared with sham) and natriuretic responses (3-fold compared with sham) to ENaC inhibitor benzamil in the rats with CHF. Absence of renal nerves produced a greater contribution of ENaC in sodium retention in rats with CHF. These results suggest that the increased expression of renal ENaC subunits may contribute to the renal sodium and water retention observed during CHF.

scholarly journals Renal denervation improves sodium excretion in rats with chronic heart failure: effects on expression of renal ENaC and AQP2

2019 ◽  
Vol 317 (5) ◽  
pp. H958-H968 ◽  
Author(s):  
Hong Zheng ◽  
Xuefei Liu ◽  
Kenichi Katsurada ◽  
Kaushik P. Patel
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Sodium Channels ◽  
Renal Denervation ◽  
Water Retention ◽  
Renal Cortex ◽  
Renal Nerves ◽  
Coronary Artery Ligation ◽  
Epithelial Sodium Channels ◽  
Aquaporin 2

Previously we have shown that increased expression of renal epithelial sodium channels (ENaC) may contribute to the renal sodium and water retention observed during chronic heart failure (CHF). The goal of this study was to examine whether renal denervation (RDN) changed the expressions of renal sodium transporters ENaC, sodium-hydrogen exchanger-3 proteins (NHE3), and water channel aquaporin 2 (AQP2) in rats with CHF. CHF was produced by left coronary artery ligation in rats. Four weeks after ligation surgery, surgical bilateral RDN was performed. The expression of ENaC, NHE3, and AQP2 in both renal cortex and medulla were measured. As a functional test for ENaC activation, diuretic and natriuretic responses to ENaC inhibitor benzamil were monitored in four groups of rats (Sham, Sham+RDN, CHF, CHF+RDN). Western blot analysis indicated that RDN (1 wk later) significantly reduced protein levels of α-ENaC, β-ENaC, γ-ENaC, and AQP2 in the renal cortex of CHF rats. RDN had no significant effects on the protein expression of kidney NHE3 in both Sham and CHF rats. Immunofluorescence studies of kidney sections confirmed the reduced signaling of ENaC and AQP2 in the CHF+RDN rats compared with the CHF rats. There were increases in diuretic and natriuretic responses to ENaC inhibitor benzamil in rats with CHF. RDN reduced the diuretic and natriuretic responses to benzamil in CHF rats. These findings suggest a critical role for renal nerves in the enhanced expression of ENaC and AQP2 and subsequent pathophysiology of renal sodium and water retention associated with CHF. NEW & NOTEWORTHY This is the first study to show in a comprehensive way that renal denervation initiated after a period of chronic heart failure reduces the expression of epithelial sodium channels and aquaporin 2 leading to reduced epithelial sodium channel function and sodium retention.

Increased expression of ENaC subunits and increased apical targeting of AQP2 in the kidneys of spontaneously hypertensive rats

2005 ◽  
Vol 289 (5) ◽  
pp. F957-F968 ◽  
Author(s):  
Soo Wan Kim ◽  
Weidong Wang ◽  
Tae-Hwan Kwon ◽  
Mark A. Knepper ◽  
Jørgen Frøkiær ◽  
...  
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Water Retention ◽  
Collecting Duct ◽  
Tubular Dysfunction ◽  
Renal Tubular Dysfunction ◽  
Protein Abundance ◽  
Hypertensive Rats ◽  
Outer Medulla ◽  
Spontaneously Hypertensive ◽  
Medullary Collecting Duct

In models of genetic hypertension, renal tubular dysfunction could be involved in the increased sodium and water reabsorption. However, the molecular basis for the increased renal sodium and water retention remains largely undefined in spontaneously hypertensive rats (SHR). We hypothesized that dysregulation of renal epithelial sodium channels (ENaC), sodium (co)transporters, or aquaporin-2 (AQP2) could be involved in the pathogenesis of hypertension in SHR. Six-week-old or twelve-week-old SHR and corresponding age-matched Wistar-Kyoto control rats (WKY) were studied. In both SHR groups, systolic blood pressure was markedly increased, whereas urine output, creatinine clearance, and urinary sodium excretion were decreased compared with corresponding WKY. Moreover, urine osmolality and urine-to-plasma osmolality ratio were increased compared with WKY. Semiquantitative immunoblotting demonstrated that the protein abundance of β- and γ-subunits of ENaC was increased in the cortex and outer stripe of the outer medulla and inner stripe of the outer medulla (ISOM) in SHR, whereas α-ENaC abundance was increased in ISOM. Immunoperoxidase microscopy confirmed the increased labeling of β-ENaC and γ-ENaC subunits in the late distal convoluted tubule, connecting tubule, and cortical and outer medullary collecting duct segments. In contrast, subcellular localization of α-ENaC, β-ENaC, and γ-ENaC was not changed. Expression of sodium/hydrogen exchanger type 3, bumetanide-sensitive Na-K-2Cl cotransporter, and thiazide-sensitive Na-Cl cotransporter was not altered in SHR. AQP2 levels were increased in the ISOM in SHR, and immunoperoxidase microscopy demonstrated an increased apical labeling of AQP2 in the inner medullary collecting duct in SHR. These results suggest that the increased protein abundance of ENaC subunits as well as the increased apical targeting of AQP2 may contribute to renal sodium and water retention observed during the development of hypertension in SHR.

scholarly journals Development of Severe Hyponatremia due to Salt-Losing Nephropathy after Esophagectomy for Esophageal Cancer

2009 ◽  
Vol 2009 ◽  
pp. 1-4
Author(s):  
Katsunobu Yoshioka ◽  
Minako Nishio ◽  
Soichi Sano ◽  
Katsunobu Sakurai ◽  
Keiko Yamagami ◽  
...  
Keyword(s):  
Esophageal Cancer ◽  
Collecting Duct ◽  
Venous Pressure ◽  
Isotonic Saline ◽  
Tubular Dysfunction ◽  
Renal Tubular Dysfunction ◽  
Cortical Collecting Duct ◽  
Laboratory Findings ◽  
Renal Tubular ◽  
Sodium Correction

A 72-year-old woman was admitted to our hospital for esophagectomy for esophageal cancer. On the third postoperative day, she developed polyuria (3.8 L/day), massive natriuresis, hyponatremia (112 mEq/L), hyperkalemia (5.6 mEq/L), and decreased central venous pressure, which was refractory to isotonic saline infusion. Laboratory findings indicated proximal tubular injury (high urinaryβ2-microglobulin, coexistence of hypouricemia) together with reduced aldosterone action at the cortical collecting duct. A diagnosis of salt-losing nephropathy was made and sodium correction was done with 3% saline and fludrocortisone. She responded well to therapy. The cause of hyponatremia was considered renal tubular dysfunction together with elevated antidiuretic hormone level. Postoperatively, it is important to look for the development of salt-losing nephropathy.

Renal Sodium Handling in Relation to Environmental and Genetic Factors in Untreated Chinese

2020 ◽  
Author(s):  
Yuan-Yuan Kang ◽  
Yi-Bang Cheng ◽  
Qian-Hui Guo ◽  
Chang-Sheng Sheng ◽  
Qi-Fang Huang ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Multiple Testing ◽  
Genetic Factors ◽  
Blood Pressure Monitoring ◽  
Lithium Concentration ◽  
Tubular Dysfunction ◽  
Renal Tubular Dysfunction ◽  
Renal Sodium Handling ◽  
Renal Tubular ◽  
Sodium Handling

Abstract Background We investigated proximal and distal renal tubular sodium handling, as assessed by fractional excretion of lithium (FELi) and fractional distal reabsorption rate of sodium (FDRNa), in relation to environmental and genetic factors in untreated patients. Methods Our study participants were suspected hypertensive patients being off antihypertensive medication for ≥2 weeks and referred for 24-hour ambulatory blood pressure monitoring. We collected serum and 24-hour urine for measurement of sodium, creatinine and lithium concentration, and calculated FELi and FDRNa. We genotyped 19 SNPs associated with renal sodium handling or blood pressure using the ABI SNapShot method. Results The 1409 participants (664 men, 47.1%) had a mean (±SD) age of 51.0±10.5 years. After adjustment for host factors, both FELi and FDRNa were significantly (P≤0.01) associated with season and humidity, explaining ~1.3% and ~3.5% of the variance, respectively. FELi was highest in autumn and lowest in summer and intermediate in spring and winter (P=0.007). FDRNa was also highest in autumn but lowest in winter and intermediate in spring and summer (P<0.001). Neither FELi nor FDRNa was associated with outdoor temperature or atmospheric pressure (P≥0.13). After adjustment for host and environmental factors and Bonferroni multiple testing, among the 19 studied genetic variants, only rs12513375 was significantly associated with FELi and FDRNa (P≤0.004) and explained about 1.7% of the variance. Conclusions Renal sodium handling as measured by endogenous lithium clearance was sensitive to major environmental and genetic factors. Our finding is towards the use of these indexes for the definition of renal tubular dysfunction.

scholarly journals Tenofovir disoproxil fumarate-associated renal tubular dysfunction

AIDS ◽  
2017 ◽  
Vol 31 (9) ◽  
pp. 1297-1301 ◽  
Author(s):  
Ryan Samuels ◽  
Carla Roca Bayerri ◽  
John A. Sayer ◽  
D. Ashley Price ◽  
Brendan A.I. Payne
Keyword(s):  
Tenofovir Disoproxil Fumarate ◽  
Tubular Dysfunction ◽  
Renal Tubular Dysfunction ◽  
Renal Tubular

Proximal Renal Tubular Dysfunction Related to Antiretroviral Therapy Among HIV-Infected Patients in an HIV Clinic in Mexico

2015 ◽  
Vol 29 (4) ◽  
pp. 181-185 ◽  
Author(s):  
Karen Andrade-Fuentes ◽  
José A. Mata-Marín ◽  
José I. López-De León ◽  
Bulmaro Manjarrez-Téllez ◽  
Jorge L. Sandoval Ramírez ◽  
...  
Keyword(s):  
Antiretroviral Therapy ◽  
Tubular Dysfunction ◽  
Renal Tubular Dysfunction ◽  
Proximal Renal Tubular Dysfunction ◽  
Renal Tubular

Induction of neonatal renal tubular dysfunction by transplacentally acquired IgG from a mother with Sjögren syndrome

1985 ◽  
Vol 107 (4) ◽  
pp. 566-569 ◽  
Author(s):  
Stanley C. Jordan ◽  
Rebecca Sakai ◽  
Michael A. Tabak ◽  
Robert B. Ettenger ◽  
Arthur H. Cohen ◽  
...  
Keyword(s):  
Sjögren Syndrome ◽  
Tubular Dysfunction ◽  
Renal Tubular Dysfunction ◽  
Sjogren Syndrome ◽  
Renal Tubular

Prenatal and Early Postnatal Intoxication by Inorganic Mercury Resulting from the Maternal Use of Mercury Containing Soap

1987 ◽  
Vol 6 (3) ◽  
pp. 253-256 ◽  
Author(s):  
R. Lauwerys ◽  
Ch. Bonnier ◽  
Ph. Evrard ◽  
J. Ph. Gennart ◽  
A. Bernard
Keyword(s):  
Inorganic Mercury ◽  
Tubular Dysfunction ◽  
Renal Tubular Dysfunction ◽  
Lactation Period ◽  
Foetal Life ◽  
Renal Tubular ◽  
Black Boy

A case of slight renal tubular dysfunction associated with cataract and anaemia was diagnosed in a 3-month-old black boy in whom high levels of mercury were found in blood and urine. Several arguments suggest that the renal, ocular and haematological defects may have resulted from exposure to mercury during foetal life and the 1-month lactation period due to the extensive use of inorganic mercury containing cosmetics by the mother.

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