Contribution of Na<sup>+</sup>‐H<sup>+</sup> exchange to sodium reabsorption in the loop of Henle: a microperfusion study in rats

Shirley, David G.; Walter, S. J.; Unwin, Robert J.; Giebisch, Gerhard

doi:10.1111/j.1469-7793.1998.243by.x

Cited by 7 publications

(11 citation statements)

References 22 publications

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“…NKCC2-mediated Na ϩ reabsorption generates a lumen-positive PD TE , partly due to apical recycling of K ϩ . The Na ϩ /H ϩ exchanger also contributes to the apical Na ϩ entry, but the role is relatively minor and it does not generate lumen-positive PD TE (23). Several pieces of evidence indicate that the effect of KS-WNK1 on Na ϩ reabsorption in cTAL is at least in large part through inhibition of NKCC2.…”

Section: Discussionmentioning

confidence: 97%

Kidney-specific WNK1 inhibits sodium reabsorption in the cortical thick ascending limb

Cheng

Truong

Baum

et al. 2012

American Journal of Physiology-Renal Physiology

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Kidney-specific WNK1 (KS-WNK1) is a variant of full-length WNK1. Previous studies have reported that KS-WNK1 is predominantly expressed in the distal convoluted tubule (DCT) where it regulates sodium-chloride cotransporter. The role of KS-WNK1 in other nephron segments is less clear. Here, we measured the expression of KS-WNK1 transcript in microdissected renal tubules and found that KS-WNK1 was most abundant in the DCT, followed by cortical thick ascending limb (cTAL), connecting tubule, and cortical collecting duct. A high K(+) diet enhanced the expression of KS-WNK1 in the DCT and cTAL, selectively. It has been reported that a high-K diet suppresses Na(+) reabsorption in TAL. To understand the role of KS-WNK1 in Na(+) transport in cTAL and the regulation by dietary K(+), we examined Na(+) reabsorption using in vitro microperfusion in cTAL isolated from KS-WNK1-knockout mice and wild-type littermates fed either a control-K(+) or high-K(+) diet. Furosemide-sensitive Na(+) reabsorption in cTAL was higher in KS-WNK1-knockout (KO) mice than in wild-type. A high-K(+) diet inhibited Na(+) reabsorption in cTAL from wild-type mice, but the inhibition was eliminated in KS-WNK1-KO mice. We further examined the role of KS-WNK1 using transgenic mice that overexpress KS-WNK1. Na(+) reabsorption in cTAL was lower in transgenic than in wild-type mice. In whole animal clearance studies, a high-K(+) diet increased daily urine volume and urinary Na(+) and K(+) excretion in wild-type mice, which was blunted in KS-WNK1-KO mice. Thus KS-WNK1 inhibits Na(+) reabsorption in cTAL and mediates the inhibition of Na(+) reabsorption in the segment by a high-K diet.

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Section: Discussionmentioning

confidence: 97%

Kidney-specific WNK1 inhibits sodium reabsorption in the cortical thick ascending limb

Cheng

Truong

Baum

et al. 2012

American Journal of Physiology-Renal Physiology

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“…It has been shown that the use of this perfusate almost abolishes fluid reabsorption by the perfused loop [15,17]. It has been shown that the use of this perfusate almost abolishes fluid reabsorption by the perfused loop [15,17].…”

Section: Methodsmentioning

confidence: 97%

Localization of diuretic effects along the loop of Henle: an in vivo microperfusion study in rats

et al. 2000

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In order to clarify the effects on sodium reabsorption in the loop of Henle of methazolamide (a carbonic anhydrase inhibitor), chlorothiazide and the loop diuretics frusemide and bumetanide, superficial loops were perfused in vivo in anaesthetized rats and the individual diuretics were included in the perfusate. Differentiation between effects in the pars recta and in the thick ascending limb of Henle (TALH) was achieved by comparing responses to the diuretics when using a standard perfusate, designed to mimic native late proximal tubular fluid, and a low-sodium perfusate, designed to block net sodium reabsorption in the pars recta. With the standard perfusate, methazolamide caused decreases in sodium reabsorption (J(Na)) and water reabsorption (J(V)); with the low-sodium perfusate, a modest effect on J(Na) persisted, suggesting that carbonic anhydrase inhibition reduces sodium reabsorption in both the pars recta and the TALH. The effects of chlorothiazide were very similar to those of methazolamide with both the standard and low-sodium perfusates, suggesting that chlorothiazide also inhibits sodium reabsorption in the pars recta and TALH, perhaps through inhibition of carbonic anhydrase. With the standard perfusate, both frusemide and bumetanide produced the expected large decreases in J(Na), but J(V) was also lowered. With the low-sodium perfusate, the inhibitory effects of the loop diuretics, particularly those of frusemide, were substantially reduced, while net potassium secretion was found. These observations indicate that a significant component of the effect of frusemide (and possibly of bumetanide) on overall sodium reabsorption is located in the pars recta, and that loop diuretics induce potassium secretion in the TALH.

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“…The use of the low-Na + perfusate in the present study has allowed us to gauge the full extent of the barium-induced reduction in Na + reabsorption in the TALH per se. We found that when barium was present the residual Na + reabsorption (149 ± 23 pmol min _1 ) was little greater than that attributable to luminal Na + -H + exchange (Shirley et al 1998b). However, even under these conditions, neither net K + reabsorption nor the concentration of K + in the collectate was significantly reduced.…”

Section: Discussionmentioning

confidence: 65%

“…It has been shown by Peterson et al (1993) and confirmed by us (Shirley et al 1998b) that the use of this perfusate almost abolishes fluid reabsorption (J V ) in the perfused loop, the residual J V being attributable to water reabsorption in the thin descending limb of Henle. Both groups have also shown that the addition of loop diuretics to the perfusate (thus blocking…”

Section: Low-na + Perfusatementioning

confidence: 70%

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Effects of the Potassium Channel Blocker Barium on Sodium and Potassium Transport in the Rat Loop of Henle In Vivo

Walter

Shirley

Folkerd

et al. 2001

Experimental Physiology

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In vitro evidence suggests that the ‘recycling’ of K+ ions through luminal K+ channels in the thick ascending limb of the loop of Henle (TALH) is essential for the normal operation of the luminal Na+‐K+‐2Cl− co‐transporter. In the present study these channels were investigated in vivo by perfusing superficial loops of Henle in anaesthetised rats with and without the K+ channel blocker barium. Using a standard perfusate, intraluminal barium (5 mmol l−1) reduced sodium reabsorption (JNa) from 1887 ± 50 to 1319 ± 53 pmol min−1 (P < 0.001). When the experiment was repeated using a low‐Na+ perfusate, designed to inhibit reabsorption in the pars recta (the initial segment of the loop of Henle), a similar reduction in JNa was observed (from 698 ± 47 to 149 ± 23 pmol min−1, P < 0.001), strongly suggesting that the effect of barium is localised to the TALH. The magnitude of the reduction in JNa during blockade of K+ channels confirms the importance of K+ recycling in facilitating Na+ reabsorption in the TALH in vivo. However, the reduction in JNa was not associated with a fall in the K+ concentration of the fluid collected at the early distal tubule. When bumetanide, an inhibitor of the Na+‐K+‐2Cl− co‐transporter, was included in the low‐Na+ perfusate, net K+ secretion was observed. Addition of barium to this perfusate reduced, but did not abolish, the secretion, suggesting that bumetanide‐induced K+ secretion results partly from paracellular transport.

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Contribution of Na⁺‐H⁺ exchange to sodium reabsorption in the loop of Henle: a microperfusion study in rats

Cited by 7 publications

References 22 publications

Kidney-specific WNK1 inhibits sodium reabsorption in the cortical thick ascending limb

Kidney-specific WNK1 inhibits sodium reabsorption in the cortical thick ascending limb

Localization of diuretic effects along the loop of Henle: an in vivo microperfusion study in rats

Effects of the Potassium Channel Blocker Barium on Sodium and Potassium Transport in the Rat Loop of Henle In Vivo

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Contribution of Na+‐H+ exchange to sodium reabsorption in the loop of Henle: a microperfusion study in rats

Cited by 7 publications

References 22 publications

Kidney-specific WNK1 inhibits sodium reabsorption in the cortical thick ascending limb

Kidney-specific WNK1 inhibits sodium reabsorption in the cortical thick ascending limb

Localization of diuretic effects along the loop of Henle: an in vivo microperfusion study in rats

Effects of the Potassium Channel Blocker Barium on Sodium and Potassium Transport in the Rat Loop of Henle In Vivo

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Contribution of Na⁺‐H⁺ exchange to sodium reabsorption in the loop of Henle: a microperfusion study in rats