Modulation of Na-K-ATPase activity in the mouse medullary thick ascending limb of Henle. Effects of mineralocorticoids and sodium.

Grossman, E.; Hebert, Steven C.

doi:10.1172/jci113399

Cited by 25 publications

(3 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…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. Similarly, in collecting duct, chronic amiloride inhibition of apical sodium channels blocks mineralocorticoid stimulation of Na/ K-ATPase (22,23).…”

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.

View full text Add to dashboard Cite

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).

show abstract

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.

View full text Add to dashboard Cite

show abstract

“…No other correlation was found between con-pellets have been accepted as a reliable method of adtinuous variables. Leaking (bursting location) occurred ministering drugs continuously for long periods of time in the preanastomotic segment of the colon in all but [8,9]. The perioperative administration (6 weeks preone specimen in the steroid group, and in this rat leak-operatively and 8 or 12 days postoperatively) approxiage occurred at the anastomosis.…”

Section: Respectively After Pellet Insertion and Were Excludedmentioning

confidence: 99%

Chronic Perioperative Steroids and Colonic Anastomotic Healing in Rats

Rio

Beck

Opelka

1996

Journal of Surgical Research

View full text Add to dashboard Cite

“…Related studies have also focused on the effects of a chronic increase in salt delivery to the loop. Feeding rats a high-salt diet for 5 d leads to an increase in the relative abundance of both the apical NaK2Cl transporter and an increase in the basolateral Na,K-ATPase ␣1 (30); the increase in TALH Na,K-ATPase activity can be prevented by treating rats with the NaK2Cl inhibitor furosemide (31,32), evidence for a causal link between chronic salt delivery to the TALH stimulating increased apical transport (by NaK2Cl) and driving an increase in basolateral sodium pump activity. Is there any adaptive rationale for an animal on a high-salt diet to reabsorb more salt in the loop of Henle?…”

Section: Discussionmentioning

confidence: 99%

Downstream Shift in Sodium Pump Activity along the Nephron during Acute Hypertension

Magyar¹,

Zhang²,

Holstein‐Rathlou³

et al. 2001

Journal of the American Society of Nephrology

View full text Add to dashboard Cite

Abstract. Acute hypertension rapidly inhibits proximal tubule (PT) Na,K-ATPase activity and sodium reabsorption 30 to 40%, increasing sodium and volume delivery to the thick ascending loop of Henle (TALH) and macula densa, providing the error signal for tubuloglomerular feedback. The hypothesis was tested in rats that an acute increase in sodium and volume delivery to the TALH would acutely increase outer medulla Na,K-ATPase activity. Flow to the TALH was increased by either (1) elevating BP (102 to 160 mmHg) for 5 min by constricting arteries (hypertension) or (2) inhibiting PT sodium and volume reabsorption with the carbonic anhydrase inhibitor benzolamide: 2 mg/kg in 300 mM NaHCO3at 50 μl/min for 5 to 7 min. Both stimuli increased urine output and lithium clearance three- to four-fold and increased basolateral Na,K-ATPase activity about 40%. In homogenates, acute hypertension increased medullary Na,K-ATPase activity from 20 ± 3.5 to 27 ± 6.4 μmol Pi/mg protein per h while decreasing renal cortex activity from 10.9 ± 0.9 to 6.5 ± 0.7. Hypertension and benzolamide also doubled medullary alkaline phosphatase activity. As chronic hypertension develops in the young spontaneously hypertensive rat, medullary Na,K-ATPase activity similarly increases. In conclusion, there is a rapid activation of medullary Na,K-ATPase activity during acute hypertension that can be explained by the increase in sodium and volume flow to the region independent of hypertension. That is, the glomerulotubular balance response in the loop of Henle is accompanied by increased Na,K-ATPase activity. The rapid, downstream shift in Na,K-ATPase activity during acute hypertension contributes the driving force for activating TGF (by inhibition in the PT) and minimizes changes in distal sodium delivery (by activation in the TALH).

show abstract

Modulation of Na-K-ATPase activity in the mouse medullary thick ascending limb of Henle. Effects of mineralocorticoids and sodium.

Cited by 25 publications

References 40 publications

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

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

Chronic Perioperative Steroids and Colonic Anastomotic Healing in Rats

Downstream Shift in Sodium Pump Activity along the Nephron during Acute Hypertension

Contact Info

Product

Resources

About