scholarly journals Hypotonic treatment evokes biphasic ATP release across the basolateral membrane of cultured renal epithelia (A6)

2002 ◽  
Vol 545 (2) ◽  
pp. 543-555 ◽  
Author(s):  
Danny Jans ◽  
S. P. Srinivas ◽  
Etienne Waelkens ◽  
Andrei Segal ◽  
Els Larivière ◽  
...  
2004 ◽  
Vol 14 (4-6) ◽  
pp. 431-440 ◽  
Author(s):  
Thomas Ludwig ◽  
Hans Oberleithner

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Mette G. Christensen ◽  
Marianne Skals ◽  
Steen Fagerberg ◽  
Randi G. Bjaelde ◽  
Jens Leipziger ◽  
...  

1992 ◽  
Vol 1110 (2) ◽  
pp. 209-217 ◽  
Author(s):  
John H. Miller ◽  
James M. Mullin ◽  
Elizabeth McAvoy ◽  
Arnost Kleinzeller

2013 ◽  
Vol 304 (10) ◽  
pp. C1013-C1026 ◽  
Author(s):  
María V. Espelt ◽  
Felicitas de Tezanos Pinto ◽  
Cora L. Alvarez ◽  
Germán Sanchez Alberti ◽  
Jeremías Incicco ◽  
...  

Hypotonicity triggered in human hepatoma cells (Huh-7) the release of ATP and cell swelling, followed by volume regulatory decrease (RVD). We analyzed how the interaction between those processes modulates cell volume. Cells exposed to hypotonic medium swelled 1.5 times their basal volume. Swelling was followed by 41% RVD40 (extent of RVD after 40 min of maximum), whereas the concentration of extracellular ATP (ATPe) increased 10 times to a maximum value at 15 min. Exogenous apyrase (which removes di- and trinucleotides) did not alter RVD, whereas exogenous Na+-K+-ATPase (which converts ATP to ADP in the extracellular medium) enhanced RVD40 by 2.6 times, suggesting that hypotonic treatment alone produced a basal RVD, whereas extracellular ADP activated RVD to achieve complete volume regulation (i.e., RVD40 ≈100%). Under hypotonicity, addition of 2-(methylthio)adenosine 5′-diphosphate (2MetSADP; ADP analog) increased RVD to the same extent as exposure to Na+-K+-ATPase and the same analog did not stimulate RVD when coincubated with MRS2211, a blocker of ADP receptor P2Y13. RT-PCR and Western blot analysis confirmed the presence of P2Y13. Cells exhibited significant ectoATPase activity, which according to RT-PCR analysis can be assigned to ENTPDase2. Both carbenoxolone, a blocker of conductive ATP release, and brefeldin A, an inhibitor of exocytosis, were able to partially decrease ATPe accumulation, pointing to the presence of at least two mechanisms for ATP release. Thus, in Huh-7 cells, hypotonic treatment triggered the release of ATP. Conversion of ATPe to ADPe by ENTPDase 2 activity facilitates the accumulated ADPe to activate P2Y13 receptors, which mediate complete RVD.


1990 ◽  
Vol 14 ◽  
pp. 76
Author(s):  
G GSTRAUNTHALER ◽  
D STEINMASSL ◽  
W PFALLER

2004 ◽  
Vol 286 (6) ◽  
pp. F1054-F1058 ◽  
Author(s):  
Peter Komlosi ◽  
Janos Peti-Peterdi ◽  
Amanda L. Fuson ◽  
Attila Fintha ◽  
Laszlo Rosivall ◽  
...  

One component of the macula densa (MD) tubuloglomerular feedback (TGF) signaling pathway may involve basolateral release of ATP through a maxi-anion channel. Release of ATP has previously been studied during a maximal luminal NaCl concentration ([NaCl]L) stimulus (20–150 mmol/l). Whether MD ATP release occurs during changes in [NaCl]L within the physiological range (20–60 mmol/l) has not been examined. Also, because TGF is known to be enhanced by low dietary salt intake, we examined the pattern of MD ATP release from salt-restricted rabbits. Fluorescence microscopy, with fura 2-loaded cultured mouse mesangial cells as biosensors, was used to assess ATP release from the isolated, perfused thick ascending limb containing the MD segment. The mesangial biosensor cells, which contain purinergic receptors and elevate intracellular Ca2+ concentration ([Ca2+]i) on ATP binding, were placed adjacent to the MD basolateral membrane. Elevations in [NaCl]L between 0 and 80 mmol/l, in 20-mmol/l increments, caused stepwise increases in [Ca2+]i, with the highest increase at [NaCl]L of ∼60 mmol/l. Luminal furosemide at 10−4 mol/l blocked ATP release, which suggests that the efflux of ATP required MD Na-2Cl-K cotransport. A low-salt diet for 1 wk increased the magnitude of [NaCl]L-dependent elevations in biosensor [Ca2+]i by twofold, whereas high-salt intake had no effect. In summary, ATP release occurs over the same range of [NaCl]L (20–60 mmol/l) previously reported for TGF responses, and, similar to TGF, ATP release was enhanced by dietary salt restriction. Thus these two findings are consistent with the role of MD ATP release as a signaling component of the TGF pathway.


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