ArticleAmerican journal of physiology. Renal physiology2009
Changes of renal AQP2, ENaC, and NHE3 in experimentally induced heart failure: response to angiotensin II AT1 receptor blockade.
Article in American journal of physiology. Renal physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 47 citations in OpenAlex.
- When the Heart Hurts the Kidneys: From Flow to Translational Future.Seminars in nephrology · 2025Review
- Sodium-glucose cotransporter 2 inhibitors and heart failure: the best timing for the right patient.Heart failure reviews · 2023Review
- Amelioration of Hypertension by Oryeongsan through Improvements of Body Fluid and Sodium Balance: Roles of the Renin-Angiotensin System and Atrial Natriuretic Peptide System.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Sodium-Glucose Co-transporter 2 Inhibitors in the Failing Heart: a Growing Potential.Cardiovascular drugs and therapy · 2020Review
- Glucocorticoids Reverse Diluted Hyponatremia Through Inhibiting Arginine Vasopressin Pathway in Heart Failure Rats.Journal of the American Heart Association · 2020Article
- DAPA-HF trial: dapagliflozin evolves from a glucose-lowering agent to a therapy for heart failure.Drugs in context · 2020Review
- 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 · 2019Article
- Protection of the kidney with sodium-glucose cotransporter 2 inhibitors: potential mechanisms raised by the large-scaled randomized control trials.Clinical and experimental nephrology · 2019Review
- SGLT2 Inhibitors and Cardiovascular Outcomes: Current Perspectives and Future Potentials.Current diabetes reports · 2018Review
- Urinary Proteolytic Activation of Renal Epithelial Na+ Channels in Chronic Heart Failure.Hypertension (Dallas, Tex. : 1979) · 2016Article
- Effects of Qili Qiangxin Capsule on AQP2, V2R, and AT1R in Rats with Chronic Heart Failure.Evidence-based complementary and alternative medicine : eCAM · 2015Article
- Article
- Regulatory roles of nitric oxide and angiotensin II on renal tubular transport.World journal of nephrology · 2014Review
- Molecular mechanisms and signaling pathways of angiotensin II-induced muscle wasting: potential therapeutic targets for cardiac cachexia.The international journal of biochemistry & cell biology · 2013Review
- Angiotensin II inhibits satellite cell proliferation and prevents skeletal muscle regeneration.The Journal of biological chemistry · 2013Article
- Regulation of transport in the connecting tubule and cortical collecting duct.Comprehensive Physiology · 2012Review
- AT1 receptors in the collecting duct directly modulate the concentration of urine.Journal of the American Society of Nephrology : JASN · 2011Article
- Increased renal ENaC subunits and sodium retention in rats with chronic heart failure.American journal of physiology. Renal physiology · 2011Article
- Water and sodium regulation in heart failure.Electrolyte & blood pressure : E & BP · 2009Article
- The role of renal water channels in health and disease.Molecular aspects of medicineReview
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Authors and funding
8 authors at 7 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heart failure (HF) was induced by ligation of the left anterior descending artery (LAD). Left ventricular end-diastolic pressure (LVEDP) >25 mmHg (at day 23 after LAD ligation) was the inclusion criterion. The rats were divided into three groups: sham-operated (Sham, n = 23, LVEDP: 5.6 +/- 0.6 mmHg), HF (n = 14, LVEDP: 29.4 +/- 1.4 mmHg), and candesartan (1 mg.kg(-1).day(-1) sc)-treated HF (HF + Can, n = 9, LVEDP: 29.2 +/- 1.2 mmHg). After 7 days (i.e., 29 days after LAD ligation) semiquantitative immunoblotting revealed increased abundance of inner medulla aquaporin-2 (AQP2) and AQP2 phosphorylated at Ser(256) (p-AQP2) in HF. There was also markedly enhanced apical targeting of AQP2 and p-AQP2 in inner medullary collecting duct (IMCD) in HF compared with Sham rats, shown by immunocytochemistry. Candesartan treatment significantly reversed the increases in both AQP2 and p-AQP2 expression and targeting. In contrast, there were only modest changes in other collecting duct segments. Semiquantitative immunoblots revealed increased expression of type 3 Na(+)/H(+) exchanger (NHE3) and Na(+)-K(+)-2Cl(-) cotransporter (NKCC2) in kidneys from HF compared with Sham rats: both effects were reversed or prevented by candesartan treatment. The protein abundance of alpha-epithelial sodium channel (alpha-ENaC) was increased while beta-ENaC and gamma-ENaC expression was decreased in the cortex and outer stripe of the outer medulla in HF compared with Sham rats, which was partially reversed by candesartan treatment. These findings strongly support an important role of angiotensin II in the pathophysiology of renal water and sodium retention associated with HF.
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