Secondary effect of aldosterone on Na-KATPase activity in the rabbit cortical collecting tubule.

Petty, Kevin J.; Kokko, Juha P.; Marver, Diana

doi:10.1172/jci110405

Cited by 195 publications

(62 citation statements)

References 42 publications

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“…As reported earlier (17)(18)(19), short term aldosterone (3 h) increased the maximal hydrolytic activity of the Na,K-ATPase by ϳ200% (ADX control, 323 Ϯ 80; ADX aldosterone, 940 Ϯ 150 pmol ATP ϫ mm Ϫ1 ϫ h Ϫ1 ; n ϭ 9; p Ͻ 0.01). We performed Western blotting to test whether or not this increase in enzyme activity could be explained by an increase in the cellular pool of the Na,K-ATPase.…”

Section: Short Term Aldosterone Increases In Vivo Nak-atpase Hydrolysupporting

confidence: 80%

“…Concerning the effect of aldosterone on the Na,K-ATPase, measurements performed two decades ago on cortical collecting ducts (CCD) of adrenalectomized rats have shown that aldosterone restores within 1-3 h the Na,K-ATPase hydrolytic activity V max and/or the number of ouabain binding sites (17)(18)(19)(20)(21). The nature of this effect was not known because the data could not distinguish between the possibilities that additional Na ϩ pump units are synthesized, that Na ϩ pumps are activated in situ, or that Na ϩ pumps are recruited/translocated from an intracellular pool to the cell surface.…”

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confidence: 99%

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Short Term Effect of Aldosterone on Na,K-ATPase Cell Surface Expression in Kidney Collecting Duct Cells

Summa¹,

Mordasini²,

Roger³

et al. 2001

Journal of Biological Chemistry

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Aldosterone controls extracellular volume and blood pressure by regulating Na ؉ reabsorption, in particular by epithelia of the distal nephron. A main regulatory site of this transcellular transport is the epithelial sodium channel (ENaC) that mediates luminal Na ؉ influx. The Na,K-ATPase (Na ؉ pump) that coordinately extrudes Na ؉ across the basolateral membrane is known to be regulated by short term aldosterone as well. We now show that in the cortical collecting duct (CCD) from adrenalectomized rats, the increase in Na,K-ATPase activity (approximately 3-fold in 3 h), induced by a single aldosterone injection, can be fully accounted by the increase in Na,K-ATPase cell surface expression (؉ 497 ؎ 35%). The short term aldosterone action was further investigated in cultured mouse collecting duct principal cells mpkCCD cl4 . Within 2 h, maximal Na,K-ATPase function assessed by Na ؉ pump current (I p ) measurements and Na,K-ATPase cell surface expression were increased by 20 -50%. Aldosterone did not modify the Na ؉ dependence of the Na ؉ pumps and induced transcription-and translation-dependent actions on pump surface expression and current independently of ENaC-mediated Na ؉ influx. In summary, short term aldosterone directly increases the cell surface expression of preexisting Na ؉ pumps in kidney CCD target cells. Thus, aldosterone controls Na ؉ reabsorption in the short term not only by regulating the apical cell surface expression of ENaC (Loffing, J., Zecevic, M., Feraille, E., Kaissling, B., Asher, C., Rossier, B. C., Firestone, G. L., Pearce, D., and Verrey, F. (2001) Am. J. Physiol. 280, F675-F682) but also by coordinately acting on the basolateral cell surface expression of the Na,K-ATPase.

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Section: Short Term Aldosterone Increases In Vivo Nak-atpase Hydrolysupporting

confidence: 80%

mentioning

confidence: 99%

Short Term Effect of Aldosterone on Na,K-ATPase Cell Surface Expression in Kidney Collecting Duct Cells

Summa¹,

Mordasini²,

Roger³

et al. 2001

Journal of Biological Chemistry

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“…4 that the loss of cotransporter precedes that of pump. Several studies in both mTAL and collecting duct have demonstrated that chronic reductions in apical sodium entry can diminish basolateral Na/K-ATPase activity in the presence of aldosterone stimulation (21)(22)(23). For example, in mTAL, Grossman and Hebert (21 ) demonstrated that mineralocorticoid-induced increases in pump activity could be prevented by chronic inhibition of the apical cotransporter using furosemide.…”

Section: Resultsmentioning

confidence: 99%

“…For example, in mTAL, Grossman and Hebert (21 ) demonstrated that mineralocorticoid-induced increases in pump activity could be prevented by chronic inhibition of the apical cotransporter using furosemide. Similarly, in collecting duct, chronic amiloride inhibition of apical sodium channels blocks mineralocorticoid stimulation of Na/ K-ATPase (22,23). By contrast, in the presence of normal aldosterone levels, reductions of Na+ entry did not lower Na/ K-ATPase activity below basal levels (23).…”

Section: Resultsmentioning

confidence: 99%

Transport defects of rabbit medullary thick ascending limb cells in obstructive nephropathy.

Hwang¹,

Haas²,

Harris³

et al. 1993

J. Clin. Invest.

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To characterize the sodium transport defect responsible for salt wasting in obstructive nephropathy, the major sodium transporters in the medullary thick ascending limb (mTAL), the apical Na-K-2CI cotransporter and the basolateral Na-KATPase, were studied in fresh suspensions of mTAL cells and outer medulla plasma membranes prepared from obstructed and untreated kidneys. Oxygen consumption (Qo2) studies in intact cells revealed marked reductions in the inhibitory effects of both furosemide and ouabain on Qo2 in cells from obstructed, as compared with control animals, indicating a reduction in activities of both the Na-K-2CI cotransporter and the Na-K-ATPase. Saturable [3Hlbumetanide binding was reduced in membranes isolated from obstructed kidneys, but the Kd for 13H Ibumetanide was unchanged, indicating a decrease in the number of functional luminal Na-K-2CI cotransporters in obstructed mTAL. Ouabain sensitive Na-K-ATPase activity in plasma membranes was also reduced, and immunoblots using specific monoclonal antibodies directed against the a and ,B subunits of rabbit Na-K-ATPase showed decreased amounts of both subunits in outer medullas of obstructed kidney. A significant decrease in I3HIbumetanide binding was detected after 4 h of ureteral obstruction, whereas Na-K-ATPase activity at this time was still not different from control. We conclude that ureteral obstruction reduces the amounts of both luminal Na-K-2CI cotransporter and basolateral Na-K-ATPase in mTAL of obstructed kidney and that these reductions contribute to the salt wasting observed after release of obstruction. (J. Clin. Invest. 1993. 91:21-28).

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“…The potassium load in the diet has been shown previously to increase renal Na-K-ATPase activity in non-adx (intact) animals (1) where changes in the enzyme activity have been localized mainly to the CCD (4,5). However, an increase in the plasma K+ concentration also increases the secretion ofaldosterone (7,8) is a strong stimulus for increasing Na-K-ATPase activity in the CCD (6,13,14). In the present study we have demonstrated that Na-K-ATPase activity in the CCD and CNT can also be increased by increasing the dietary K+ intake in the absence of aldosterone.…”

Section: Discussionmentioning

confidence: 97%

Renal adaptation to potassium in the adrenalectomized rabbit. Role of distal tubular sodium-potassium adenosine triphosphatase.

Garg¹,

Narang²

1985

J. Clin. Invest.

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Potassium secretion and sodium-potassium adenosine triphosphatase (Na-K-ATPase) activity in the distal nephron segments are known to be influenced by the dietary intake of KV. This has been attributed to a change in the plasma aldosterone level, which also influences K+ secretion and Na-K-ATPase activity in the distal nephron. To investigate whether or not dietary K+ can modulate Na-K-ATPase activity in the distal nephron independently of aldosterone, we determined Na-K-ATPase activity in four distinct nephron segments of adrenalectomized (adx) rabbits given four specific diets for 1 wk before experimentation. Na-K-ATPase activity was determined by a fluorometric microassay in which ATP hydrolysis is coupled to NADH oxidation. The nephron segments examined were the distal convoluted tubule (DCI), the connecting tubule (CNT), the cortical collecting duct (CCD), and the outer medullary collecting duct (MCD). All diets were similar in composition except for their K+ contents, which were 100, 300, 500, and 700 meq/kg in groups 14, respectively. In these adx animals, Na-K-ATPase activity increased >200% in the CCD as the dietary intake of K+ increased. There was a linear relationship between K+ excretion and the enzyme activity in this segment. There was a 50% increase in Na-K-ATPase activity in the CNT as the dietary intake of K+ increased in adx animals. However, there were no significant differences in Na-K-ATPase activities in the DCT and MCD among the four treatment groups. It is concluded that dietary K+ intake can influence Na-K-ATPase activity in the CCD and CNT independently of plasma aldosterone levels.

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Secondary effect of aldosterone on Na-KATPase activity in the rabbit cortical collecting tubule.

Cited by 195 publications

References 42 publications

Short Term Effect of Aldosterone on Na,K-ATPase Cell Surface Expression in Kidney Collecting Duct Cells

Short Term Effect of Aldosterone on Na,K-ATPase Cell Surface Expression in Kidney Collecting Duct Cells

Transport defects of rabbit medullary thick ascending limb cells in obstructive nephropathy.

Renal adaptation to potassium in the adrenalectomized rabbit. Role of distal tubular sodium-potassium adenosine triphosphatase.

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