Upregulation of calbindin D28k in the late distal tubules in the potassium-loaded adrenalectomized mouse kidney

Kobayashi, Miyuki; Yasuoka, Yukiko; Sato, Yuichi; Zhou, Ming; Abe, Hiroshi; Kawahara, Katsumasa; Okamoto, Hirotsugu

doi:10.1007/s10157-011-0414-4

Cited by 9 publications

(5 citation statements)

References 36 publications

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“…The P[aldo] for Con mice of 239 pg/ml ( Table 1 ) using ELISA was close to the values of 322 pg/ml [ 17 ] and 400 pg/ml [ 34 ] of previous studies using radioimmunoassay (RIA). For HK diet, our value of 753 pg/ml using ELISA was less than the value of 1797 ± 630 using RIA [ 32 ]; however, the SEM of the RIA value indicates some readings in the range of our value.…”

Section: Discussionmentioning

confidence: 58%

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Low Na, High K Diet and the Role of Aldosterone in BK-Mediated K Excretion

Cornelius

Wen

et al. 2015

PLoS ONE

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A low Na, high K diet (LNaHK) is associated with a low rate of cardiovascular (CV) disease in many societies. Part of the benefit of LNaHK relies on its diuretic effects; however, the role of aldosterone (aldo) in the diuresis is not understood. LNaHK mice exhibit an increase in renal K secretion that is dependent on the large, Ca-activated K channel, (BK-α with accessory BK-β4; BK-α/β4). We hypothesized that aldo causes an osmotic diuresis by increasing BK-α/β4-mediated K secretion in LNaHK mice. We found that the plasma aldo concentration (P[aldo]) was elevated by 10-fold in LNaHK mice compared with control diet (Con) mice. We subjected LNaHK mice to either sham surgery (sham), adrenalectomy (ADX) with low aldo replacement (ADX-LA), or ADX with high aldo replacement (ADX-HA). Compared to sham, the urinary flow, K excretion rate, transtubular K gradient (TTKG), and BK-α and BK-β4 expressions, were decreased in ADX-LA, but not different in ADX-HA. BK-β4 knockout (β4KO) and WT mice exhibited similar K clearance and TTKG in the ADX-LA groups; however, in sham and ADX-HA, the K clearance and TTKG of β4KO were less than WT. In response to amiloride treatment, the osmolar clearance was increased in WT Con, decreased in WT LNaHK, and unchanged in β4KO LNaHK. These data show that the high P[aldo] of LNaHK mice is necessary to generate a high rate of BK-α/β4-mediated K secretion, which creates an osmotic diuresis that may contribute to a reduction in CV disease.

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Section: Discussionmentioning

confidence: 58%

“…Mice on LNaHK [ 9 ], or HK [ 8 , 32 , 33 ] exhibit a urinary flow that is 5-fold that of Con mice. A high urine volume is necessary to dilute the K in the CNT/CCD and excrete K at a high rate because the concentration of K that can be secreted in the CNT/CCD is limited to approximately 120 mM [ 9 ].…”

Section: Resultsmentioning

confidence: 99%

Low Na, High K Diet and the Role of Aldosterone in BK-Mediated K Excretion

Cornelius

Wen

et al. 2015

PLoS ONE

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“…Our data are in line with observations in humans with type 1 aldosterone deficiency, who are usually still able to adapt renal K + excretion and to stay more or less in K + balance. 38 Likewise, adrenalectomized animals 23,24,39 were shown to augment renal K + excretion in response to an increased dietary K + intake, although usually at the expense of more or less elevated plasma K + levels. Previous studies on adrenalectomized rats and rabbits indicated that a high-K + diet increases renal Na + and K + channel activities independent from aldosterone.…”

Section: Discussionmentioning

confidence: 99%

“…22,23 However, adrenalectomy is not always complete and residual plasma aldosterone levels may persist. 24 Moreover, local aldosterone producing systems may exist in many organs including the kidney. 25 Hence, we used mice with targeted inactivation of the aldosterone synthase (AS) 26 to analyze in detail the cellular and molecular mechanisms involved in the regulation of K + homeostasis under conditions of complete aldosterone deficiency.…”

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confidence: 99%

Mechanisms of Renal Control of Potassium Homeostasis in Complete Aldosterone Deficiency

Todkar

Picard²,

Loffing‐Cueni³

et al. 2015

Journal of the American Society of Nephrology

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Aldosterone-independent mechanisms may contribute to K + homeostasis. We studied aldosterone synthase knockout (AS 2/2 ) mice to define renal control mechanisms of K + homeostasis in complete aldosterone deficiency. AS 2/2 mice were normokalemic and tolerated a physiologic dietary K + load (2% K + , 2 days) without signs of illness, except some degree of polyuria. With supraphysiologic K + intake (5% K + ), AS 2/2 mice decompensated and became hyperkalemic. High-K + diets induced upregulation of the renal outer medullary K + channel in AS 2/2 mice, whereas upregulation of the epithelial sodium channel (ENaC) sufficient to increase the electrochemical driving force for K + excretion was detected only with a 2% K + diet. Phosphorylation of the thiazide-sensitive NaCl cotransporter was consistently lower in AS 2/2 mice than in AS +/+ mice and was downregulated in mice of both genotypes in response to increased K + intake.Inhibition of the angiotensin II type 1 receptor reduced renal creatinine clearance and apical ENaC localization, and caused severe hyperkalemia in AS 2/2 mice. In contrast with the kidney, the distal colon of AS 2/2 mice did not respond to dietary K + loading, as indicated by Ussing-type chamber experiments. Thus, renal adaptation to a physiologic, but not supraphysiologic, K + load can be achieved in aldosterone deficiency by aldosteroneindependent activation of the renal outer medullary K + channel and ENaC, to which angiotensin II may contribute. Enhanced urinary flow and reduced activity of the thiazide-sensitive NaCl cotransporter may support renal adaptation by activation of flow-dependent K + secretion and increased intratubular availability of Na + that can be reabsorbed in exchange for K + secreted.

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“…Kidney sections were immuno-stained, as described previously [ 7 , 28 ]. In brief, the sections were blocked with 5% normal goat serum and reacted with rabbit polyclonal anti-human Epo antibody (sc-7956, 1:50; Santa Cruz Biotechnology, Santa Cruz, CA, USA), followed by Histofine Simple Stain MAX-PO (414341F; Nichirei Bioscience, Tokyo, Japan).…”

Section: Methodsmentioning

confidence: 99%

Effects of Angiotensin II on Erythropoietin Production in the Kidney and Liver

et al. 2021

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The kidney is a main site of erythropoietin production in the body. We developed a new method for the detection of Epo protein by deglycosylation-coupled Western blotting. Detection of deglycosylated Epo enables the examination of small changes in Epo production. Using this method, we investigated the effects of angiotensin II (ATII) on Epo production in the kidney. ATII stimulated the plasma Epo concentration; Epo, HIF2α, and PHD2 mRNA expression in nephron segments in the renal cortex and outer medulla; and Epo protein expression in the renal cortex. In situ hybridization and immunohistochemistry revealed that ATII stimulates Epo mRNA and protein expression not only in proximal tubules but also in collecting ducts, especially in intercalated cells. These data support the regulation of Epo production in the kidney by the renin–angiotensin–aldosterone system (RAS).

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Upregulation of calbindin D28k in the late distal tubules in the potassium-loaded adrenalectomized mouse kidney

Abstract: Upregulation of calbindin in the late distal tubule suggests that Ca(2+)-dependent K transport may function as an alternative mechanism for urinary K excretion in ADX mice.

Cited by 9 publications

References 36 publications

Low Na, High K Diet and the Role of Aldosterone in BK-Mediated K Excretion

Low Na, High K Diet and the Role of Aldosterone in BK-Mediated K Excretion

Mechanisms of Renal Control of Potassium Homeostasis in Complete Aldosterone Deficiency

Effects of Angiotensin II on Erythropoietin Production in the Kidney and Liver

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