Effect of acid lumen pH on potassium transport in renal cortical collecting tubules

Jf, Boudry; Lc, Stoner; Burg, M. B.

doi:10.1152/ajplegacy.1976.230.1.239

Cited by 54 publications

(24 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…11 26 transepithelial Na ϩ flux was unaffected by changes in luminal pH. Similarly, Na ϩ absorption in the superficial distal tubule was unchanged after a 1-hour infusion of NaHCO 3 .…”

Section: Absorption Of Namentioning

confidence: 86%

Pendrin Modulates ENaC Function by Changing Luminal HCO3 −

Pech¹,

Pham²,

Hong³

et al. 2010

Journal of the American Society of Nephrology

102

View full text Add to dashboard Cite

The epithelial Na ϩ channel, ENaC, and the Cl Ϫ /HCO 3 Ϫ exchanger, pendrin, mediate NaCl absorption within the cortical collecting duct and the connecting tubule. Although pendrin and ENaC localize to different cell types, ENaC subunit abundance and activity are lower in aldosterone-treated pendrin-null mice relative to wild-type mice. Because pendrin mediates HCO 3 Ϫ secretion, we asked if increasing distal delivery of HCO 3 Ϫ through a pendrin-independent mechanism "rescues" ENaC function in pen- 21: 192821: -194121: , 201021: . doi: 10.1681 Pendrin, encoded by Slc26a4, is an aldosterone-sensitive Cl Ϫ /HCO 3 Ϫ exchanger that mediates Cl Ϫ absorption and HCO 3 Ϫ secretion in the cortical collecting duct (CCD). 1-3 During NaCl restriction, pendrin-null mice excrete more NaCl than wild-type mice, which increases apparent vascular volume contraction and lowers BP. [3][4][5] The chloruresis observed in pendrin-null mice during NaCl restriction likely results from the absence of pendrin-mediated Cl Ϫ absorption. 3,4 However, because pendrin does not transport Na ϩ , the cause of the natriuresis observed in the mutant mice was explored further. After either dietary NaCl restriction or the administration of aldosterone, renal ENaC function and ENaC subunit abundance were lower in pendrin-null mice than in wildtype mice. 5 In particular, ␥ ENaC abundance was reduced in kidneys from pendrin-null mice relative to wild-type mice. However, how pendrin J Am Soc Nephrol

show abstract

“…11 26 transepithelial Na ϩ flux was unaffected by changes in luminal pH. Similarly, Na ϩ absorption in the superficial distal tubule was unchanged after a 1-hour infusion of NaHCO 3 .…”

Section: Absorption Of Namentioning

confidence: 86%

Pendrin Modulates ENaC Function by Changing Luminal HCO3 −

Pech¹,

Pham²,

Hong³

et al. 2010

Journal of the American Society of Nephrology

102

View full text Add to dashboard Cite

show abstract

“…Another factor responsible for the increased K excretion might be the increased amounts of HCO3 in the distal tubule which would behave as a nonreabsorbable anion further increasing luminal negativity leading to increased K secretion (53,57). Fi.rthermore, K secretion in the cortical collecting tubule has been shown to increase when the luminal pH is raised (58). Finally, increased…”

Section: Resultsmentioning

confidence: 99%

Effects of Acetazolamide on Proximal Tubule Cl, Na, and HCO3 Transport in Normal and Acidotic Dogs during Distal Blockade

Chou¹,

Porush²,

Slater³

et al. 1977

J. Clin. Invest.

View full text Add to dashboard Cite

A B S T R A C T It has been suggested that the establishment of a tubular fluid to plasma chloride gradient in the late proximal tubule by the reabsorption of bicarbonate (and other anions) in the early proximal tubule is responsible for a significant part of sodium chloride and water reabsorption in the proximal tubule. In the present study the effects of acetazolamide on proximal tubule water and electrolyte excretion were examined in 6 normal dogs and 10 chronic ammonium chloride-loaded dogs during distal blockade produced by ethacrynic acid and chlorothiazide administration. During distal blockade control urine/plasma osmolality and urine/plasma sodium were close to unity in all experiments. Urine/plasma chloride and urine/plasma bicarbonate were 1.21+0.02 and 0.75+0.07 in normal and 1.24+0.01 and 0.04+0.01 in acidotic dogs, respectively. After the administration of acetazolamide (20 mg/kg i.v.), there was a significant increase in urine flow, absolute and fractional excretion of sodium, bicarbonate, and chloride in all animals. Associated with these effects, urine/plasma osmolality and urine/ plasma sodium remained unchanged but urine/plasma chloride decreased significantly to 1.15±0.01 in normal and to 1.19+0.01 in acidotic dogs. In acidotic dogs there was a significant correlation between the increase in bicarbonate, sodium, or chloride excretion after acetazolamide and the plasma bicarbonate level (range 6.8-12.5 meq/liter). These data demonstrate a significant effect of acetazolamide on bicarbonate, sodium, and chloride reabsorption in the proximal tubule even in the face of severe acidosis. Moreover, the data suggest that the decrease in chloride reabsorption (and accompanying sodium) after acetazolamide is related to the decrease in bicarbonate reabsorption and the associated decrease in the transtubular chloride gradient.

show abstract

“…In vitro studies on the isolated perfused CCT of the rabbit have demonstrated the existence of active potassium secretion in this segment (23)(24)(25)(26)(27). The ability of patients and experimental animals with renal disease to maintain potassium homeostasis despite significant reductions on functioning renal mass (1,4,(14)(15)(16)(17)(18)(19)(20)(21)(22)(28)(29)(30)(31)(32) suggests that nephron sites which normally secrete potassium are able to augment this secretion to maintain potassium balance in chronic uremia.…”

Section: Discussionmentioning

confidence: 99%