Renal Ion-Translocating ATPases: The P-Type Family

Horisberger, Jean‐Daniel; Doucet, Alain

doi:10.1016/b978-012088488-9.50006-1

Cited by 3 publications

(6 citation statements)

References 426 publications

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“…Molecular cloning has revealed that colonic and gastric H,K-ATPase share 60–70% sequence homology and that gastric H,K-ATPase and colonic H,K-ATPase contain HKα1 (type I K-ATPase) and HKα2 (type III K-ATPase), respectively [39]. Several early studies have suggested that gastric H,K-ATPase was involved in renal K absorption from K-depleted animals [12, 28, 142].…”

Section: Apical K Transport In the Cnt And Collecting Ductmentioning

confidence: 99%

“…It had been reported that Rb influx, an index of K transport, increased in the OMCD from rabbits on a K-deficient diet and that this effect was abolished by inhibition of gastric H,K-ATPase [147]. However, the late investigations have shown that colonic H,K-ATPase, rather than gastric H,K-ATPase, is mainly responsible for renal K reabsorption and that gastric H,K-ATPase is involved in mediating K-dependent proton secretion in collecting duct [39]. First, application of ouabain inhibited Sch-28080-sensitive Rb 2+ absorption in OMCD [146].…”

Section: Apical K Transport In the Cnt And Collecting Ductmentioning

confidence: 99%

“…The notion that high K intake increases K secretion by an aldosterone-independent mechanism is also suggested by the observation that high K intake continues, albeit at a reduced rate, to stimulate K secretion in the isolated perfusion CCD from adrenalectomized rabbit [68]. HK intake inhibits K reabsorption not only by decreasing colonic H,K-ATPase expression [39] but also through enhancing apical K channel activity in IC [51]. This may indirectly affect the activity of H,K-ATPase by enhancing K recycling across the apical membrane, thereby diminishing net K reabsorption.…”

Section: Regulation Of K Excretion By K Dietmentioning

confidence: 99%

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Regulation of potassium (K) handling in the renal collecting duct

Wang

Giebisch

2008

Pflugers Arch - Eur J Physiol

141

115

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This review provides an overview of the molecular mechanisms of K transport in the mammalian connecting tubule (CNT) and cortical collecting duct (CCD), both nephron segments responsible for the regulation of renal K secretion. Aldosterone and dietary K intake are two of the most important factors regulating K secretion in the CNT and CCD. Recently, angiotensin II (AngII) has also been shown to play a role in the regulation of K secretion. In addition, genetic and molecular biological approaches have further identified new mechanisms by which aldosterone and dietary K intake regulate K transport. Thus, the interaction between serum-glucocorticoid-induced kinase 1 (SGK1) and with-no-lysine kinase 4 (WNK4) plays a significant role in mediating the effect of aldosterone on ROMK (Kir1.1), an important apical K channel modulating K secretion. Recent evidence suggests that WNK1, mitogen-activated protein kinases such as P38, ERK, and Src family protein tyrosine kinase are involved in mediating the effect of low K intake on apical K secretory channels. KeywordsPotassium transport; Potassium channel; Potassium secretion; Angiotensin; Aldosterone; K channel; Kidney Overview of K transport mechanism in CNT and CCDMaintaining plasma K within a narrow physiological range is essential for the function of neurons, cardiac myocytes, and skeletal muscles. The kidney plays a key role in regulating K excretion by completely filtering K in the glomerulus, reabsorbing K extensively along the proximal tubule and thick ascending limb, secreting K in the connecting tubule (CNT) and cortical collecting duct (CCD), and reabsorbing K in outer medullary collecting duct (OMCD). Two morphological distinct cells, principal cell (PC) and intercalated cell (IC), are present in the CNT and CCD [29,75], and it is generally accepted that PC and IC are responsible for K secretion and for K absorption, respectively [27,30]. Figure 1 is a cell model illustrating the K transport mechanism under control conditions (normal K intake) in both PC and IC in the CCD [29,74,75]. K secretion takes place by a two-step process: K enters the cell via the basolateral Na,K-ATPase and is secreted into the lumen through apical K channels along a favorable electrochemical gradient [76,101]. K absorption is achieved by K entering the cell across the apical membrane through a luminal H,K-ATPase and leaving the cell across the basolateral membrane along a favorable K electrochemical gradient [19,21,33]. Although H,K-ATPase is Luminal Na transport provides normally an important driving force for K secretion [97], but recent evidence has shown that K secretion may continue when luminal Na transport is compromised. As demonstrated in microperfused rabbit CCD, K secretion may continue, albeit at a reduced rate, in the absence of luminal Na [69]. Since inhibition of basolateral Na/H exchanger significantly decreases such K secretion in the absence of luminal Na, it is most likely that Na recycling across the basolateral membrane through Na/H exchange supplies enough ...

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Section: Apical K Transport In the Cnt And Collecting Ductmentioning

confidence: 99%

Section: Apical K Transport In the Cnt And Collecting Ductmentioning

confidence: 99%

Section: Regulation Of K Excretion By K Dietmentioning

confidence: 99%

See 1 more Smart Citation

Regulation of potassium (K) handling in the renal collecting duct

Wang

Giebisch

2008

Pflugers Arch - Eur J Physiol

141

115

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“…This distribution has been observed in several species, such as rats, mice, rabbits, and humans (Wagner et al 2004). An additional primary active mechanism of proton secretion has also been reported: a nonelectrogenic H + /K + -ATPase (Wingo and Smolka 1995;Horisberger and Doucet 2000;Gumz et al 2010). Two isoforms of H + /K + -ATPase have been cloned from rat gastric mucosa and colon, respectively.…”

Section: Discussionmentioning

confidence: 97%

Stimulation of calcium-sensing receptor increases biochemical H⁺-ATPase activity in mouse cortex and outer medullary regions

Casare

Milan

Fernández

2014

Can. J. Physiol. Pharmacol.

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The aim of this project was to investigate the interaction between the calcium-sensing receptor (CaSR) and proton extrusion by the V-ATPase and gastric-like isoform of the H(+)/K(+)-ATPase in the mouse nephron. Biochemical activity of H(+)- ATPases was analysed using a partially purified membrane fraction of mouse cortex and outer medullary region. The V-ATPase activity (sensitive to 10(-7) mol·L(-1) bafilomycin) from the cortical and outer medullary region was significantly stimulated by increasing the [Formula: see text] (outside Ca(2+)), in a dose-dependent pattern. Gastric H(+)/K(+)-ATPase activity (sensitive to 10(-5) mol·L(-1) Schering 28080) was also sensitive to changes in [Formula: see text] levels. A significant increase in V-ATPase activity was also observed when CaSR was stimulated with agonists such as 300 μmol·L(-1) Gd(3+) and 200 μmol·L(-1) neomycin, both in the cortex and outer medulla. The cortical and outer medullary gastric H(+)/K(+)-ATPase activity was also stimulated by Gd(3+) and neomycin. Finally, cortical V-ATPase activity was significantly stimulated by 10(-9) mol·L(-1) angiotensin II, and the stimulation of CaSR in the presence of angiotensin significantly enhanced this effect, suggesting that an interaction in the intracellular signaling pathways is involved. In summary, CaSR stimulation enhances the biochemical activity of V-ATPase and gastric H(+)/K(+)-ATPase in both the cortical and outer medullary region of mouse kidney.

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“…Both Na ϩ -K ϩ -ATPase and H ϩ -K ϩ -ATPases belong to the P-type family of ATPases, which are characterized by the transient phosphorylation of an aspartyl residue during the functional cycle (14). P-type ATPases also share their require-ment for an additional ␤-subunit to form a functional transporter.…”

Section: Discussionmentioning

confidence: 99%

ANP-stimulated Na⁺ secretion in the collecting duct prevents Na⁺ retention in the renal adaptation to acid load

Cheval

Bakouh

Walter

et al. 2019

American Journal of Physiology-Renal Physiology

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We have recently reported that type A intercalated cells of the collecting duct secrete Na+ by a mechanism coupling the basolateral type 1 Na+-K+-2Cl− cotransporter with apical type 2 H+-K+-ATPase (HKA2) functioning under its Na+/K+ exchange mode. The first aim of the present study was to evaluate whether this secretory pathway is a target of atrial natriuretic peptide (ANP). Despite hyperaldosteronemia, metabolic acidosis is not associated with Na+ retention. The second aim of the present study was to evaluate whether ANP-induced stimulation of Na+ secretion by type A intercalated cells might account for mineralocorticoid escape during metabolic acidosis. In Xenopus oocytes expressing HKA2, cGMP, the second messenger of ANP, increased the membrane expression, activity, and Na+-transporting rate of HKA2. Feeding mice with a NH4Cl-enriched diet increased urinary excretion of aldosterone and induced a transient Na+ retention that reversed within 3 days. At that time, expression of ANP mRNA in the collecting duct and urinary excretion of cGMP were increased. Reversion of Na+ retention was prevented by treatment with an inhibitor of ANP receptors and was absent in HKA2-null mice. In conclusion, paracrine stimulation of HKA2 by ANP is responsible for the escape of the Na+-retaining effect of aldosterone during metabolic acidosis.

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Renal Ion-Translocating ATPases: The P-Type Family

Cited by 3 publications

References 426 publications

Regulation of potassium (K) handling in the renal collecting duct

Regulation of potassium (K) handling in the renal collecting duct

Stimulation of calcium-sensing receptor increases biochemical H⁺-ATPase activity in mouse cortex and outer medullary regions

ANP-stimulated Na⁺ secretion in the collecting duct prevents Na⁺ retention in the renal adaptation to acid load

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Renal Ion-Translocating ATPases: The P-Type Family

Cited by 3 publications

References 426 publications

Regulation of potassium (K) handling in the renal collecting duct

Regulation of potassium (K) handling in the renal collecting duct

Stimulation of calcium-sensing receptor increases biochemical H+-ATPase activity in mouse cortex and outer medullary regions

ANP-stimulated Na+ secretion in the collecting duct prevents Na+ retention in the renal adaptation to acid load

Contact Info

Product

Resources

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Stimulation of calcium-sensing receptor increases biochemical H⁺-ATPase activity in mouse cortex and outer medullary regions

ANP-stimulated Na⁺ secretion in the collecting duct prevents Na⁺ retention in the renal adaptation to acid load