scholarly journals Kinetics of luminal acidification in cortical tubules of the rat kidney.

1977 ◽  
Vol 267 (3) ◽  
pp. 571-599 ◽  
Author(s):  
G Giebisch ◽  
G Malnic ◽  
G B De Mello ◽  
M De Mello Aires
Keyword(s):  
Rat Kidney ◽  
Kinetics Of

Differentiation of Na(+)-K+ pumps of low-K+ sheep red blood cells is promoted by Lp membrane antigens

1993 ◽  
Vol 265 (1) ◽  
pp. C99-C105 ◽  
Author(s):  
Z. C. Xu ◽  
P. B. Dunham ◽  
B. Dyer ◽  
R. Blostein
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Rat Kidney ◽  
Striking Increase ◽  
Sheep Red Blood Cells ◽  
High K ◽  
Membrane Antigens ◽  
Low K ◽  
Kinetics Of

Na(+)-K+ pumps of red blood cells from sheep of the low-K+ (LK) phenotype undergo differentiation during circulation, manifested in part by a striking increase in sensitivity to inhibition by intracellular K+ (Ki). Pumps of red blood cells from sheep from the allelic phenotype, high K+ (HK), do not undergo this type of maturation. The hypothesis was tested that the Lp antigen, found on LK but not HK cells, is responsible for the maturation of LK pumps. Lp antigens have been shown to inhibit LK pumps because anti-Lp antibody stimulates the pumps by relieving inhibition by the antigen. Lp antigens were recently shown to be molecular entities separate from Na(+)-K+ pumps [Xu, Z.-C., P. Dunham, J. Munzer, J. Silvius, and R. Blostein. Am. J. Physiol. 263 (Cell Physiol. 32): C1007-C1014, 1992]. The test of the hypothesis was to modify the Lp antigens of immature LK red blood cells with two kinds of treatments, anti-Lp antibody and trypsinization (which cleaves Lp), and to observe the effects of these treatments on maturation of pumps during culture of the cells in vitro. Both of these treatments prevented the maturation of the kinetics of the pumps to the Ki-sensitive pattern, supporting the hypothesis that interaction of the pumps with Lp antigens is responsible for the maturation of the pumps. Strong supportive evidence came from experiments on Na(+)-K+ pumps from rat kidney delivered into immature LK sheep red blood cells by microsome fusion.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals TGN38/41 recycles between the cell surface and the TGN: brefeldin A affects its rate of return to the TGN.

1993 ◽  
Vol 4 (1) ◽  
pp. 93-105 ◽  
Author(s):  
B Reaves ◽  
M Horn ◽  
G Banting
Keyword(s):  
Plasma Membrane ◽  
Specific Binding ◽  
Rat Kidney ◽  
Brefeldin A ◽  
Integral Membrane Protein ◽  
Intracellular Compartments ◽  
Normal Rat ◽  
Golgi Network ◽  
Lumenal Domain ◽  
Kinetics Of

TGN38 and TGN41 are isoforms of an integral membrane protein (TGN38/41) that is predominantly localized to the trans-Golgi network (TGN) of normal rat kidney cells. Polyclonal antisera to TGN38/41 have been used to monitor its appearance at, and removal from, the surface of control and Brefeldin A (BFA)-treated cells. Antibodies that recognize the lumenal domain of TGN38/41 are capable of specific binding to the surface of both control and BFA-treated cells. In both control and BFA-treated cells internalized TGN38/41 is targeted to the TGN; however, there are differences in 1) the morphology of the intracellular structures through which TGN38/41 passes and 2) the kinetics of internalization. These data demonstrate that TGN38/41 cycles between the plasma membrane and the TGN in control and BFA-treated cells and suggest that recycling pathways between the plasma membrane and the TGN exist for predominantly TGN proteins as well as those that normally cycle to other intracellular compartments. They also demonstrate that addition of BFA not only alters the morphology and localization of the TGN but also the kinetics of endocytosis.

scholarly journals An agent or agents produced by virus-transformed cells cause unregulated ruffling in untransformed cells.

1986 ◽  
Vol 102 (4) ◽  
pp. 1224-1229 ◽  
Author(s):  
S E Myrdal ◽  
N Auersperg
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Rat Kidney ◽  
Rabbit Igg ◽  
Murine Sarcoma Virus ◽  
Normal Rat ◽  
Sarcoma Virus ◽  
Epidermal Growth ◽  
Factor Type ◽  
Kinetics Of

KNRK cells (a normal rat kidney [NRK] cell line transformed by Kirsten murine sarcoma virus) in sparse culture exhibit a highly ruffled morphology, but the cause of this ruffling is unknown. In this study, we have demonstrated that the continuous, excess ruffling on KNRK cells is caused by one or more soluble agents secreted by the KNRK cells themselves. To do this study, an assay for ruffling responses in live cell cultures was defined, and its reproducibility was demonstrated. This assay permitted observation of the kinetics of ruffling responses (percentage of cells ruffled as a function of time after stimulation). This method was used to compare the kinetics of ruffling induced by insulin, epidermal growth factor, fibroblast growth factor, glucose, and KNRK cell conditioned medium (CM). Ruffling was elicited on NRK cells by each of the polypeptide mitogens and nutrients, but, in each case, this ruffling subsided spontaneously within an hour. CM from KNRK cells also caused ruffling movements on untransformed NRK cells, but this ruffling continued for at least 20 h. This response was largely blocked by premixing the KNRK cell CM with rabbit IgG against rat transforming growth factor, type alpha, (TGF-alpha). KNRK cells made quiescent (ruffle free) by a pH shift (from 7.4 to 8.4) responded to insulin, glucose, and KNRK cell CM with kinetics similar to those observed for each of these factors in NRK cells. The unusual feature for the ruffle-inducing agent(s) produced by KNRK cells was that this activity was not subject, in either NRK or KNRK cells, to the cellular off-regulation that limits the responses to insulin or glucose. Thus, the continuous ruffling of KNRK cells is caused by their own unregulated ruffle-inducing agent or agents, which appear to include TGF-alpha. This work also demonstrates that kinetic analysis of cellular responses to exogenous factors can provide new insights into the regulatory mechanisms involved in the normal limitation of these responses.

Tubular reabsorption rates for myoglobin in the isolated perfused rat kidney

1986 ◽  
Vol 70 (6) ◽  
pp. 595-599 ◽  
Author(s):  
P. J. Ratcliffe ◽  
M. P. Esnouf ◽  
J. G. G. Ledingham
Keyword(s):  
Rat Kidney ◽  
Tubular Reabsorption ◽  
Renal Tubules ◽  
Immunoglobulin Light Chain ◽  
Renal Handling ◽  
Water Excretion ◽  
Isolated Perfused Rat Kidney ◽  
Saturation Kinetics ◽  
Perfused Rat Kidney ◽  
Kinetics Of

1. The renal handling of myoglobin has been studied in the isolated perfused rat kidney. 2. Myoglobin was freely filtered. Reabsorption by the renal tubules showed saturation kinetics with a relatively low maximum rate of reabsorption (Tmax) of 27-30 μg min−1 g−1 wet wt. at a perfusate concentration of 70-80 μg/ml. Myoglobin reabsorption is therefore much less than that reported for immunoglobulin light chain or lysozyme in this model. 3. Large increases in sodium and water excretion produced by omission of oncotic agent from the perfusate did not alter the kinetics of myoglobin reabsorption. 4. The use of bovine serum albumin as oncotic agent in the perfusate prevented the tubular reabsorption of myoglobin. Small amounts of albumin are filtered by the isolated perfused kidney and it is postulated that this albumin interferes with tubular reabsorption of myoglobin.

Kinetics of the Glomerular Ultrafiltration in the Rat Kidney. An Experimental Study

1975 ◽  
Vol 95 (3) ◽  
pp. 293-300 ◽  
Author(s):  
Ö. Källskog ◽  
L. O. Lindbom ◽  
H. R. Ulfendahl ◽  
M. Wolgast
Keyword(s):  
Experimental Study ◽  
Rat Kidney ◽  
Glomerular Ultrafiltration ◽  
Kinetics Of
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