scholarly journals Na restriction activates epithelial Na channels in rat kidney through two mechanisms and decreases distal Na+ delivery

2018 ◽  
Vol 596 (16) ◽  
pp. 3585-3602 ◽  
Author(s):  
Gustavo Frindt ◽  
Lei Yang ◽  
Krister Bamberg ◽  
Lawrence G. Palmer

2004 ◽  
Vol 286 (4) ◽  
pp. F669-F674 ◽  
Author(s):  
Gustavo Frindt ◽  
Lawrence G. Palmer

Epithelial Na channels were investigated using patch-clamp techniques in connecting tubule (CNT) segments isolated from rat kidney. Cell-attached patches with Li+ in the patch pipette contained channels with conductances for inward currents of 13–16 pS and slow opening and closing kinetics, similar to properties of Na channels in the cortical collecting tubule (CCT). Macroscopic amiloride-sensitive currents ( INa) were also observed under whole cell clamp conditions. These currents were undetectable in cells from control rats but were large when the animals were infused with aldosterone (1,380 ± 340 pA/cell at a holding potential of -100 mV) or fed a high-K diet (670 ± 260 pA/cell) for 1 wk. Under both of these conditions, currents in cells of the CNT were two- to fourfold larger than currents in cells of the CCT of the same animals. In aldosterone-treated animals, currents in cells of the initial collecting tubule (iCT) were intermediate, such that the relative magnitude of INa was as follows: CNT > iCT > CCT. Quantitative analysis of the results suggests that the maximal capacity of the aggregate population of CNTs to reabsorb Na could be as high as 18 μmol/min, or ∼10% of the filtered load of Na. This capacity is ∼10 times higher than that of the CCT.



1992 ◽  
Vol 54 (1) ◽  
pp. 51-66 ◽  
Author(s):  
L G Palmer


2015 ◽  
Vol 308 (6) ◽  
pp. F572-F578 ◽  
Author(s):  
Gustavo Frindt ◽  
Lawrence G. Palmer

The acute effects of aldosterone administration on epithelial Na channels (ENaC) in rat kidney were examined using electrophysiology and immunodetection. Animals received a single injection of aldosterone (20 μg/kg body wt), which reduced Na excretion over the next 3 h. Channel activity was assessed in principal cells of cortical collecting ducts as amiloride-sensitive whole cell clamp current ( INa). INa averaged 100 pA/cell, 20–30% of that reported for the same preparation under conditions of chronic stimulation. INa was negligible in control animals that did not receive hormone. The acute physiological response correlated with changes in ENaC processing and trafficking. These effects included increases in the cleaved forms of α-ENaC and γ-ENaC, assessed by Western blot, and increases in the surface expression of β-ENaC and γ-ENaC measured after surface protein biotinylation. These changes were qualitatively and quantitatively similar to those of chronic stimulation. This suggests that altered trafficking to or from the apical membrane is an early response to the hormone and that later increases in channel activity require stimulation of channels residing at the surface.



1997 ◽  
Vol 272 (3) ◽  
pp. L407-L412 ◽  
Author(s):  
G. Yue ◽  
S. Matalon

We instilled 4 ml isotonic fluid containing trace amounts of fluorescently labeled dextran (molecular mass 150 kDa) in the lungs of rats exposed to either 85% O(2) for 7 days or to 85% O(2) for 7 days and 100% O(2) for 3 days. We withdrew the fluid every hour for a 3-h period and calculated alveolar fluid clearance (AFC) from changes in dextran concentration. Postinstillation (3 h), AFC values in the control and the two hyperoxic groups were 51 +/- 1, 63 +/- 2, and 62 +/- 3 (SE), respectively (%instilled volume; n > or = 5; P < 0.05). Addition of either 1 mM amiloride or N-ethyl-N-isopropyl amiloride (EIPA) in the instillate decreased the AFC values in all groups 3 h later to approximately 30% of instilled volume. Instillation of phenamil, an irreversible blocker of epithelial Na+ channels into the lungs of rats exposed to 85% O(2) for 7 days and 100% O(2) for 2 days, resulted in a significant increase of their extravascular lung fluid volumes 24 h later. These results demonstrate the existence of EIPA-inhibitable Na+ channels in alveolar epithelial cells in vivo and indicate that an increase in Na+ transport plays an important role in limiting the amount of alveolar edema in O(2)-damaged lungs.



2004 ◽  
Vol 280 (9) ◽  
pp. 8513-8522 ◽  
Author(s):  
Shaohu Sheng ◽  
Clint J. Perry ◽  
Ossama B. Kashlan ◽  
Thomas R. Kleyman


1996 ◽  
Vol 432 (5) ◽  
pp. 760-766 ◽  
Author(s):  
A. E. Busch ◽  
H. Suessbrich ◽  
K. Kunzelmann ◽  
A. Hipper ◽  
R. Greger ◽  
...  


2001 ◽  
Vol 276 (17) ◽  
pp. 13744-13749 ◽  
Author(s):  
Anuwat Dinudom ◽  
Kieran F. Harvey ◽  
Permsak Komwatana ◽  
Corina N. Jolliffe ◽  
John A. Young ◽  
...  


Physiology ◽  
1995 ◽  
Vol 10 (2) ◽  
pp. 61-67 ◽  
Author(s):  
LG Palmer

Epithelial Na channels help maintain Na homeostasis by controlling the rate of Na absorption by the kidney and other organs. Surprisingly, they show homology with genes involved in mechanical sensing and transduction. This suggests that epithelial Na channels and stretch-activated channels may be in the same family.



1985 ◽  
Vol 86 (1) ◽  
pp. 69-77 ◽  
Author(s):  
Kathy Lazorick ◽  
Christopher Miller ◽  
Sarah Sariban-Sohraby ◽  
Dale Benos


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