scholarly journals Ontogeny of Purinergic Receptor-Regulated Ca2+ Signaling in Mouse Cortical Collecting Duct Epithelium

2002 ◽  
Vol 12 (2-3) ◽  
pp. 75-82 ◽  
Author(s):  
Johannes Tschöp ◽  
Gerald Braun ◽  
Rene Borscheid ◽  
Michael Horster ◽  
Stephan Huber
2010 ◽  
Vol 176 (2) ◽  
pp. 630-637 ◽  
Author(s):  
Michael J. Hiatt ◽  
Larissa Ivanova ◽  
Nuria Toran ◽  
Alice F. Tarantal ◽  
Douglas G. Matsell

1996 ◽  
Vol 270 (1) ◽  
pp. F53-F60 ◽  
Author(s):  
H. P. Koster ◽  
A. Hartog ◽  
C. H. van Os ◽  
R. J. Bindels

Rabbit connecting tubule and cortical collecting duct cells were isolated by immunodissection and cultured to confluence on permeable filters and on glass coverslips. Extracellular ATP dose-dependently reduced transcellular Na+ and Ca2+ transport (half-maximal inhibitory concentration, IC50, of 0.5 +/- 0.2 and 3.2 +/- 0.5 microM), with a maximal inhibition of 57 +/- 5 and 43 +/- 4%, respectively. Purinergic receptor agonists inhibited transport with the following rank order of potency: UTP = ATP > ADP; this suggests involvement of P2u purinoceptors. ATP also caused a dose-dependent (50% effective dose, EC50, of 1.5 +/- 0.2 microM) transient increase in intracellular Ca2+ concentration ([Ca2+]i), which decreased to a sustained elevated level. In the absence of extracellular Ca2+, a similar Ca2+ transient occurred, but the sustained response was abolished. Preloading the cells with the Ca2+ chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA) completely prevented the ATP-induced Ca2+ transients, but not the ATP-induced inhibition of Na+ and Ca2+ absorption. Activation of protein kinase C (PKC) by the cell-permeable diacylglycerol analogue, 1,2-dioctanoyl-en-glycerol, mimicked ATP-induced inhibition of Na+ and Ca2+ absorption. The inhibitory effects of ATP were no longer observed after culturing cells in the presence of phorbol ester (12-O-tetradecanoylphorbol-13-acetate) for 5 days, which resulted in downregulation of cellular PKC activity.


2010 ◽  
Vol 2010 ◽  
pp. 1-9 ◽  
Author(s):  
Peter Trnka ◽  
Michael J. Hiatt ◽  
Larissa Ivanova ◽  
Alice F. Tarantal ◽  
Douglas G. Matsell

Epithelial-mesenchymal transition (EMT) has emerged in recent years as an important process in the development of organ fibrosis in many human diseases. Our previous experience in a nonhuman primate model of obstructive nephropathy suggested that EMT of collecting duct epithelium contributes to the development of interstitial fibrosis. In this study we demonstrate for the first time in humans that obstructed fetal collecting duct epithelium undergoes transition to mesenchymal phenotype, characterized by decreased expression of epithelial markers, de novo expression of mesenchymal markers with subsequent loss of cell-cell interaction, disruption of the basement membrane, and increased deposition of extracellular matrix into the expanded interstitium of the obstructed kidney. The results of this study therefore support the previous findings from animal studies and suggest that EMT of the collecting duct epithelium might contribute to the development of interstitial fibrosis in human fetal obstructive nephropathy.


1993 ◽  
Vol 44 (3) ◽  
pp. 527-536 ◽  
Author(s):  
Sabine Kloth ◽  
Joachim Aigner ◽  
Ernst Brandt ◽  
Roland Moll ◽  
Will W. Minuth

1960 ◽  
Vol 199 (6) ◽  
pp. 1215-1218 ◽  
Author(s):  
Richard H. Kessler

According to the countercurrent hypothesis urine tonicity depends largely on osmotic equilibrium of collecting duct fluid with the hypertonic interstitium of the papilla. One suggested role of ADH is that of regulating water permeability of collecting duct epithelium. In water deprivation ADH would facilitate water movement from collecting duct to the hypertonic papilla. Support for this hypothesis is offered here. These studies use the observation that ureteral clamping curtails glomerular filtration. Hence, the filtered load of NaCl from which papillary stores are derived is reduced. Accordingly, the chloride content of papillary tissues obtained from dog kidneys subsequent to several minutes of ureteral clamping was compared to those from the opposite kidney. In saline-loaded animals stasis uniformly lowered tissue chloride with the production of urine lower in chloride content and hypotonic to that of the contralateral side. These alterations were minimized following urinary stasis in animals loaded with water, mannitol or saline plus ADH.


1998 ◽  
Vol 275 (1) ◽  
pp. F25-F32 ◽  
Author(s):  
Stephan M. Huber ◽  
Michael F. Horster

Developmental expression of ion channels possibly participating in regulatory volume decrease was studied in rat embryonic ( day E17) and perinatal ( days P1–6) ureteric bud and in postnatal ( P9–14) cortical collecting duct cells in primary monolayer culture. In isotonic bath solution, whole cell conductance (in nS/10 pF) was highest in E17 (4.0 ± 0.5, n = 31) compared with P1–6 (2.0 ± 0.1, n = 16) and P9–14 (1.3 ± 0.2, n = 12) due to a decreasing contribution of a DIDS-sensitive Cl conductance, from E17 (2.8 ± 0.7, n = 12) to P1–6 (0.53 ± 0.07, n = 9) and P9–14 (0.05 ± 0.1, n = 7). Cl conductance in E17 exhibited a permselectivity of I ≈ Cl ≈ Br ≫ gluconate, and it activated time dependently. Hypotonic bath solution induced a large increase of whole cell conductance in P1–6 and in P9–14 but not in E17 (by 20.0 ± 3.7, 21.5 ± 5.5, and 4.9 ± 1.7; n = 11, 12, and 25, respectively) due to the activation of a time-dependently inactivating Cl conductance with a permselectivity of I ≥ Br > Cl ≫ gluconate. In conclusion, the expression of Cl channels, as studied in vitro, appears to shift from an apparently constitutively active embryonic to a hypotonic swelling-activated type during late embryonic development of the collecting duct.


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