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Renal denervation improves sodium excretion in rats with chronic heart failure: effects on expression of renal ENaC and AQP2.
. 2019 11 01; 317(5):H958-H968.

Abstract

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.

Authors+Show Affiliations

Division of Basic Biomedical Sciences, Sanford School of Medicine of the University of South Dakota, Vermillion, South Dakota.Division of Basic Biomedical Sciences, Sanford School of Medicine of the University of South Dakota, Vermillion, South Dakota.Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska.Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska.

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

31490733

Citation

Zheng, Hong, et al. "Renal Denervation Improves Sodium Excretion in Rats With Chronic Heart Failure: Effects On Expression of Renal ENaC and AQP2." American Journal of Physiology. Heart and Circulatory Physiology, vol. 317, no. 5, 2019, pp. H958-H968.
Zheng H, Liu X, Katsurada K, et al. Renal denervation improves sodium excretion in rats with chronic heart failure: effects on expression of renal ENaC and AQP2. Am J Physiol Heart Circ Physiol. 2019;317(5):H958-H968.
Zheng, H., Liu, X., Katsurada, K., & Patel, K. P. (2019). Renal denervation improves sodium excretion in rats with chronic heart failure: effects on expression of renal ENaC and AQP2. American Journal of Physiology. Heart and Circulatory Physiology, 317(5), H958-H968. https://doi.org/10.1152/ajpheart.00299.2019
Zheng H, et al. Renal Denervation Improves Sodium Excretion in Rats With Chronic Heart Failure: Effects On Expression of Renal ENaC and AQP2. Am J Physiol Heart Circ Physiol. 2019 11 1;317(5):H958-H968. PubMed PMID: 31490733.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Renal denervation improves sodium excretion in rats with chronic heart failure: effects on expression of renal ENaC and AQP2. AU - Zheng,Hong, AU - Liu,Xuefei, AU - Katsurada,Kenichi, AU - Patel,Kaushik P, Y1 - 2019/09/06/ PY - 2020/11/01/pmc-release PY - 2019/9/7/pubmed PY - 2020/4/9/medline PY - 2019/9/7/entrez KW - heart failure KW - renal function KW - renal nerve KW - sympathetic nerve activity SP - H958 EP - H968 JF - American journal of physiology. Heart and circulatory physiology JO - Am. J. Physiol. Heart Circ. Physiol. VL - 317 IS - 5 N2 - 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. SN - 1522-1539 UR - https://www.unboundmedicine.com/medline/citation/31490733/Renal_denervation_improves_sodium_excretion_in_rats_with_chronic_heart_failure:_effects_on_expression_of_renal_ENaC_and_AQP2_ L2 - https://journals.physiology.org/doi/10.1152/ajpheart.00299.2019?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -