ArticleAmerican journal of physiology. Renal physiology2008
Candesartan augments compensatory changes in medullary transport proteins in the diabetic rat kidney.
Article in American journal of physiology. Renal physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- Downregulation of the kidney glucagon receptor, essential for renal function and systemic homeostasis, contributes to chronic kidney disease.Cell metabolism · 2024Article
- UT-A1/A3 knockout mice show reduced fibrosis following unilateral ureteral obstruction.American journal of physiology. Renal physiology · 2020Article
- E3 ligase MDM2 mediates urea transporter-A1 ubiquitination under either constitutive or stimulatory conditions.American journal of physiology. Renal physiology · 2019Article
- Metformin improves urine concentration in rodents with nephrogenic diabetes insipidus.JCI insight · 2016Article
- Predicted consequences of diabetes and SGLT inhibition on transport and oxygen consumption along a rat nephron.American journal of physiology. Renal physiology · 2016Article
- Molecular mechanisms of urea transport in health and disease.Pflugers Archiv : European journal of physiology · 2012Review
- Chronic use of chloroquine disrupts the urine concentration mechanism by lowering cAMP levels in the inner medulla.American journal of physiology. Renal physiology · 2012Article
- Renal distal tubule proliferation and increased aquaporin 2 level but decreased urine osmolality in db/db mouse: treatment with chromium picolinate.Experimental and molecular pathology · 2012Article
- The role of nitric oxide in the dysregulation of the urine concentration mechanism in diabetes mellitus.Frontiers in physiology · 2012Article
- Collecting duct-specific knockout of adenylyl cyclase type VI causes a urinary concentration defect in mice.American journal of physiology. Renal physiology · 2012Article
- Losartan chemistry and its effects via AT1 mechanisms in the kidney.Current medicinal chemistry · 2009Review
- Candesartan Differentially Regulates Epithelial Sodium Channel in Cortex Versus Medulla of Streptozotocin-Induced Diabetic Rats.Journal of epithelial biology & pharmacology · 2009Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Volume depletion due to persistent glucosuria-induced osmotic diuresis is a significant problem in uncontrolled diabetes mellitus (DM). Angiotensin II receptor blockers (ARBs), such as candesartan, slow the progression of chronic kidney disease in patients with DM. However, mice with genetic knockout of components of the renin-angiotensin system have urine concentrating defects, suggesting that ARBs may exacerbate the volume depletion. Therefore, the effect of candesartan on UT-A1, UT-A3, NKCC2, and aquaporin-2 (AQP2) protein abundances was determined in control and 3-wk DM rats. Aldosterone levels in control rats (0.36 +/- 0.06 nM) and candesartan-treated rats (0.34 +/- 0.14 nM) were the same. DM rats had higher aldosterone levels (1.48 +/- 0.37 nM) that were decreased by candesartan (0.97 +/- 0.26 nM). Western analysis showed that UT-A1 expression was increased in DM rats compared with controls in inner medullary (IM) tip (158 +/- 13%) and base (120 +/- 25%). UT-A3 abundance was increased in IM tip (123 +/- 11%) and base (146 +/- 17%) of DM rats vs. controls. UT-A3 was unchanged in candesartan-treated control rats. In candesartan-treated DM rats, UT-A3 increased in IM tip (160 +/- 14%) and base (210 +/- 19%). Candesartan-treated DM rats had slightly higher AQP2 in IM (46%, P < 0.05) vs. control rats. NKCC2/BSC1 was increased 145 +/- 10% in outer medulla of DM vs. control rats. We conclude that candesartan augments compensatory changes in medullary transport proteins, reducing the losses of solute and water during uncontrolled DM. These changes may represent a previously unrecognized beneficial effect of type 1 ARBs in DM.
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