Changes in tubular basolateral membrane markers after chronic DOCA treatment

1983 ◽  
Vol 245 (1) ◽  
pp. F100-F109 ◽  
Author(s):  
G. El Mernissi ◽  
D. Chabardes ◽  
A. Doucet ◽  
A. Hus-Citharel ◽  
M. Imbert-Teboul ◽  
...  
Keyword(s):  
Adenylate Cyclase ◽  
Atpase Activity ◽  
Protein Content ◽  
Basolateral Membrane ◽  
Chronic Administration ◽  
Distal Nephron ◽  
Nephron Segments ◽  
Collecting Tubule ◽  
Nephron Segment ◽  
Cortical Collecting Tubule

Chronic administration of DOCA to rabbits is known to increase the surface area of the basolateral membrane and the Na-K-ATPase activity of the cortical collecting tubule (CCT). We attempted to ascertain 1) whether Na-K-ATPase is the only basolateral membrane marker induced by DOCA, and 2) whether CCT is the only nephron segment affected by this steroid. We measured the activity of Na-K-ATPase and adenylate cyclase (AC) and the protein content of nephron segments microdissected from control and DOCA-treated rabbits. Morphogenic effects of DOCA, assessed by 30-60% increases in protein content, were specifically observed in the distal convoluted tubule, CCT, and medullary collecting tubule. When expressed as a function of tubular length, Na-K-ATPase activity rose from 80 to 200% in all these segments, whereas the increments in AC of 40-70%, observed in response to four different hormones, occurred only in some of them. When expressed as a function of protein content, Na-K-ATPase activity increased but AC activity remained unchanged. This study indicates that the morphogenic action resulting from chronic DOCA administration affects the entire rabbit distal nephron. During this action Na-K-ATPase is the preferentially induced enzyme.

Characterization of K-ATPase activity in distal nephron: stimulation by potassium depletion

1987 ◽  
Vol 253 (3) ◽  
pp. F418-F423 ◽  
Author(s):  
A. Doucet ◽  
S. Marsy
Keyword(s):  
Atpase Activity ◽  
Rat Kidney ◽  
Intercalated Cells ◽  
Distal Nephron ◽  
Morphological Alterations ◽  
Nephron Segments ◽  
Collecting Tubule ◽  
K Depletion ◽  
Cortical Collecting Tubule

Intercalated cells of the distal segments of the mammalian nephron are able to reabsorb K through an active mechanism, particularly during K depletion. However, the molecular basis of this transport is unknown. Therefore, we attempted to determine whether a K-ATPase similar to K-H-ATPase described in gastric mucosa and colon might be present in segments of the distal nephron and thereby account for active K reabsorption. K-stimulated ATPase activity was detected in microdissected segments of rabbit nephron: its activity was proportional to the density of intercalated cells, since it was highest in the connecting tubule, intermediate in the cortical collecting tubule, lowest in the outer medullary collecting tubule, and was not detectable in all other nephron segments. K-ATPase had a high affinity for K (Km approximately equal to 0.2-0.4 mM), was inhibited by vanadate and omeprazole, and was insensitive to ouabain, indicating that it is different from Na+-K+-ATPase but similar to K-H-ATPase. In the rat kidney, K-ATPase was also detected in the collecting tubule and its activity was markedly increased (+100-200%) following K depletion. This stimulation occurred before morphological alterations and might therefore be a primary event responsible for K conservation during K depletion. In summary, these results demonstrate the presence of a vanadate-sensitive, ouabain-insensitive K-ATPase activity in distal nephron segments of mammalian tubules. It is suggested that K-ATPase activity originates in intercalated cells where it might account, at least in part, for K reabsorption.

Difference in the Na affinity of Na(+)-K(+)-ATPase along the rabbit nephron: modulation by K

1990 ◽  
Vol 259 (2) ◽  
pp. F246-F250 ◽  
Author(s):  
C. Barlet-Bas ◽  
L. Cheval ◽  
C. Khadouri ◽  
S. Marsy ◽  
A. Doucet
Keyword(s):  
Atpase Activity ◽  
Thick Ascending Limb ◽  
Kidney Cells ◽  
Nephron Segments ◽  
Adaptive Property ◽  
Collecting Tubule ◽  
Pump Activity ◽  
K Concentration ◽  
Cortical Collecting Tubule

The sensitivity of Na(+)-K(+)-ATPase to Na was determined in single segments of rabbit nephron isolated by microdissection. In the cortical collecting tubule (CCT), Na(+)-K(+)-ATPase was threefold more sensitive to Na (apparent K0.5 approximately 3 mM) than in proximal convoluted tubule and cortical thick ascending limb (apparent K0.5 approximately 10 mM). Furthermore, increasing K concentration from 5 to greater than 100 mM markedly reduced the affinity of the pump for Na in all three nephron segments. In fact, the main shift in Na affinity occurred when K changed from 100 to 120 mM; in the CCT, increasing K concentration from 100 to 120 mM while maintaining Na concentration at 10 mM reduced Na(+)-K(+)-ATPase activity by greater than 35%. These findings confirm that, in kidney cells as in other cells, intracellular Na limits the rate of Na(+)-K(+)-ATPase. Thus any alteration of intracellular Na concentration modifies the pump activity in a way that contributes to the restoration of intracellular Na homeostasis. This adaptive property is particularly efficient in the collecting tubule in which the apparent K0.5 of the pump for Na is close to normal intracellular Na concentration. Furthermore, changes in intracellular K concentration, which usually accompany those of Na so as to maintain the total cation concentration constant, potentiate the regulatory role of Na through modifications of its affinity for the pump.

Influence of chronic ADH treatment on adenylate cyclase and ATPase activity in distal nephron segments of diabetes insipidus Brattleboro rats

1985 ◽  
Vol 405 (3) ◽  
pp. 216-222 ◽  
Author(s):  
M. M. Trinh-Trang-Tan ◽  
L. Bankir ◽  
A. Doucet ◽  
G. El Mernissi ◽  
M. Imbert-Teboul ◽  
...  
Keyword(s):  
Adenylate Cyclase ◽  
Atpase Activity ◽  
Diabetes Insipidus ◽  
Brattleboro Rats ◽  
Distal Nephron ◽  
Nephron Segments

Expression of claudin-7 and -8 along the mouse nephron

2004 ◽  
Vol 286 (6) ◽  
pp. F1063-F1071 ◽  
Author(s):  
Wing Y. Li ◽  
Catherine L. Huey ◽  
Alan S. L. Yu
Keyword(s):  
Tight Junction ◽  
Renal Tubule ◽  
Basolateral Membrane ◽  
Paracellular Permeability ◽  
Mouse Kidney ◽  
Integral Membrane Proteins ◽  
Distal Nephron ◽  
Nephron Segments ◽  
Nephron Segment

Claudins are integral membrane proteins of the tight junction that determine the magnitude and selectivity of paracellular permeability in epithelial tissues. The mammalian renal tubule exhibits considerable heterogeneity in the permeability properties of its different segments. To determine the nephron segment localization of claudin-7 and -8, immunofluorescence staining of mouse kidney sections was performed using isoform-specific antibodies. Claudin-8 was found to be expressed primarily at the tight junction along the entire aldosterone-sensitive distal nephron and in the late segments of the thin descending limbs of long-looped nephrons. This pattern of expression is consistent with the putative role of claudin-8 as a paracellular cation barrier. By contrast, claudin-7 was found in the same nephron segments as claudin-8, but it was expressed primarily at the basolateral membrane.

Effect of metabolic acidosis and alkalosis on NEM-sensitive ATPase in rat nephron segments

1992 ◽  
Vol 262 (4) ◽  
pp. F583-F590 ◽  
Author(s):  
C. Khadouri ◽  
S. Marsy ◽  
C. Barlet-Bas ◽  
L. Cheval ◽  
A. Doucet
Keyword(s):  
Metabolic Acidosis ◽  
Atpase Activity ◽  
Thick Ascending Limb ◽  
Nephron Segments ◽  
Medullary Thick Ascending Limb ◽  
Henle's Loop ◽  
Collecting Tubule ◽  
Nephron Segment ◽  
Electrogenic Proton Pump ◽  
Chloride Treatment

An N-ethylmaleimide (NEM)-sensitive adenosinetriphosphatase (ATPase) displaying the kinetic and pharmacological properties of an electrogenic proton pump has been described in the different segments of rat nephron, where it mediates part of the active tubular proton secretion. This study was therefore designed to evaluate whether changes in urinary acidification observed during metabolic acidosis or alkalosis were associated with alterations of the activity of tubular NEM-sensitive ATPase, and if so, to localize the nephron segments responsible for these changes. Within 1 wk after the onset of ammonium chloride treatment, rats developed a metabolic acidosis, and NEM-sensitive ATPase activity was markedly increased in the medullary thick ascending limb of Henle's loop and outer medullary collecting tubule, and slightly increased in the cortical collecting tubule. Conversely, treatment with sodium bicarbonate induced a metabolic alkalosis that was accompanied by decreased NEM-sensitive ATPase activity in medullary thick ascending limb and outer medullary collecting tubule. NEM-sensitive ATPase activity was not altered in any other nephron segment tested in alkalotic and acidotic rats, i.e., the proximal tubule and the cortical thick ascending limb of Henle's loop. Changes qualitatively similar were observed as soon as 3 h after the onset of NaHCO3 or NH4Cl-loading. In the medullary collecting tubule, alterations of NEM-sensitive ATPase activity are in part due to hyperaldosteronism observed in both acidotic and alkalotic rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Na+,K+-ATPase activity and hormones in single nephron segments from nephrotic rats

1991 ◽  
Vol 80 (6) ◽  
pp. 599-604 ◽  
Author(s):  
B. Vogt ◽  
H. Favre
Keyword(s):  
Nephrotic Syndrome ◽  
Atpase Activity ◽  
Hormonal Regulation ◽  
Sodium Balance ◽  
Sodium Retention ◽  
Twofold Increase ◽  
Nephron Segments ◽  
Endogenous Ouabain ◽  
Collecting Tubule ◽  
Cortical Collecting Tubule

1. In the nephrotic syndrome the kidneys retain salt and water, which leads to oedema formation. The site of this sodium retention has been localized in the cortical collecting tubule by micropuncture studies. Whether or not this phenomenon is an intrinsic renal problem or is the consequence of changes in hormonal activities is still a matter of discussion. 2. Using the model of puromycin aminonucleoside-induced nephrotic syndrome in the rat, we measured Na+,K+-ATPase activity in nephron segments from control and nephrotic rats and investigated the regulatory role of aldosterone and endogenous-ouabain-displacing factor. 3. Nephrotic animals had a twofold increase in Na+,K+-ATPase activity in the cortical collecting tubule only (control versus nephrotic: 1065 ± 68 versus 2081 ± 274 pmol h−1 mm−1, P = 0.036), which was not modified by adrenalectomy and was independent of the kidney content of endogenous ouabain-displacing factor. Na+,K+-ATPase activity in the cortical collecting tubule correlated with the sodium balance in both control and nephrotic rats. 4. The data are consistent with the view that sodium retention in this model of the nephrotic syndrome is a primary event, i.e. an increase in sodium transport throughout the cortical collecting tubule expressed as a twofold increase in Na+,K+-ATPase activity which is no longer under hormonal regulation (aldosterone and endogenous ouabain-displacing factor).

Stimulation of Na-K-ATPase in the rat collecting tubule by two diuretics: furosemide and amiloride

1984 ◽  
Vol 247 (3) ◽  
pp. F485-F490 ◽  
Author(s):  
G. E. Mernissi ◽  
A. Doucet
Keyword(s):  
Atpase Activity ◽  
Chronic Administration ◽  
Maximal Activity ◽  
Thick Ascending Limb ◽  
Sodium Permeability ◽  
Nephron Segments ◽  
Collecting Tubule ◽  
Pump Activity ◽  
Tubule Diameter ◽  
Stimulation Of

To test whether sodium availability controls the concentration of renal Na-K-ATPase, we evaluated the effect of chronic alterations in apical membrane sodium permeability in specific nephron segments on the maximal activity of Na-K-ATPase. For this purpose Na-K-ATPase activity was determined in nephron segments microdissected from rats treated continuously for 3-8 days with either furosemide or amiloride, two diuretics known to lower the apical permeability to sodium in the thick ascending limb and the collecting tubule, respectively. Unexpectedly, Na-K-ATPase activity was decreased neither in the thick ascending limb nor in the collecting tubule after administration of either drug. In fact, both diuretics paradoxically increased the pump activity by 60-150% in the collecting tubule. This stimulation of Na-K-ATPase activity was accompanied with an enhancement of the collecting tubule diameter. Stimulation of Na-K-ATPase was identical in the collecting tubule of diuretic-treated rats receiving spironolactone. These results suggest that Na-K-ATPase maximal activity is not controlled by sodium availability or by aldosterone under these conditions and that chronic administration of furosemide or amiloride induces Na-K-ATPase activity in the collecting tubule. This effect appears to be independent of aldosterone.

Ontogenesis of hormone-dependent adenylate cyclase in isolated rat nephron segments

1984 ◽  
Vol 247 (2) ◽  
pp. F316-F325 ◽  
Author(s):  
M. Imbert-Teboul ◽  
D. Chabardes ◽  
A. Clique ◽  
M. Montegut ◽  
F. Morel
Keyword(s):  
Parathyroid Hormone ◽  
Adenylate Cyclase ◽  
Rat Kidney ◽  
Basolateral Membrane ◽  
Thick Ascending Limb ◽  
Membrane Area ◽  
Nephron Segments ◽  
Target Sites ◽  
Collecting Tubule ◽  
Kinetics Of

Ontogenesis of hormone-dependent adenylate cyclase (AC) was investigated in rat kidney by single tubule microassay between two days postnatal and adulthood. This approach allowed us to analyze the kinetics of vasopressin-sensitive AC maturation in its tubular target sites, namely the thick ascending limb and collecting tubule. It was also possible to compare in a single segment--the thick ascending limb--the kinetics of AC ontogenesis for three hormones-- vasopressin, calcitonin, and parathyroid hormone. The results show that 1) 2 days after birth AC is still poorly responsive to vasopressin, especially in the thick ascending limb. By contrast, this segment exhibits marked AC responses to calcitonin and parathyroid hormone. 2) For a given hormone, the kinetics of AC ontogenesis depends on the segment in which the receptor-enzyme complex is located. 3) For a given segment, the pattern of AC maturation is specific for each hormone. These data indicate that the process of tubular AC maturation cannot be accounted for simply by an increase in basolateral membrane area or by the synthesis of new catalytic units. More specific mechanisms must be involved that regulate independently the synthesis of each kind of hormone receptor and/or its coupling to cyclase.

scholarly journals Basolateral membrane Na(+)-independent Cl-/HCO3- exchange in the inner stripe of the rabbit outer medullary collecting tubule.

1990 ◽  
Vol 95 (2) ◽  
pp. 347-367 ◽  
Author(s):  
S R Hays ◽  
R J Alpern
Keyword(s):  
Basolateral Membrane ◽  
Cell Voltage ◽  
Complete Removal ◽  
Distal Nephron ◽  
Cell Ph ◽  
Collecting Tubule ◽  
Nephron Segment ◽  
A Cell ◽  
Segment Cell

The inner stripe of the outer medullary collecting tubule is a major distal nephron segment in urinary acidification. To examine the mechanism of basolateral membrane H+/OH-/HCO3- transport in this segment, cell pH was measured microfluorometrically in the inner stripe of the rabbit outer medullary collecting tubule perfused in vitro using the pH-sensitive fluorescent dye, (2',7')-bis(carboxyethyl)-(5,6)-carboxyfluorescein. Decreasing peritubular pH from 7.4 to 6.8 (changing [HCO3-] from 25 to 5 mM) caused a cell acidification of 0.25 +/- 0.02 pH units, while a similar luminal change resulted in a smaller cell acidification of only 0.04 +/- 0.01 pH units. Total replacement of peritubular Cl- with gluconate caused cell pH to increase by 0.18 +/- 0.04 pH units, an effect inhibited by 100 microM peritubular DIDS and independent of Na+. Direct coupling between Cl- and base was suggested by the continued presence of peritubular Cl- removal-induced cell alkalinization under the condition of a cell voltage clamp (K(+)-valinomycin). In addition, 90% of basolateral membrane H+/OH-/HCO3- permeability was inhibited by complete removal of luminal and peritubular Cl-. Peritubular Cl(-)-induced cell pH changes were inhibited two-thirds by removal of exogenous CO2/HCO3- from the system. The apparent Km for peritubular Cl- determined in the presence of 25 mM luminal and peritubular [HCO3-] was 113.5 +/- 14.8 mM. These results demonstrate that the basolateral membrane of the inner stripe of the outer medullary collecting tubule possesses a stilbene-sensitive Cl-/HCO3- exchanger which mediates 90% of basolateral membrane H+/OH-/HCO3- permeability and may be regulated by physiologic Cl- concentrations.

Renal potassium adaptation: Na-K-ATPase activity along the nephron after chronic potassium loading

1980 ◽  
Vol 238 (5) ◽  
pp. F380-F386 ◽  
Author(s):  
A. Doucet ◽  
A. I. Katz
Keyword(s):  
Atpase Activity ◽  
Major Site ◽  
Potassium Adaptation ◽  
Collecting Tubule ◽  
Nephron Segment ◽  
Potassium Clearance ◽  
Potassium Loading ◽  
Stimulation Of ◽  
Cortical Collecting Tubule

To identify nephron sites where renal potassium adaptation takes place, Na-K-ATPase was measured with a micromethod along the nephron of potassium-loaded mice. A possible role of aldosterone in this process was evaluated in K-loaded animals treated concurrently with pharmacologic doses of spironolactone. Animals fed a potassium-enriched diet for at least 2 wk excreted about 90% of ingested potassium in the urine, and fractional potassium clearance averaged 87 +/- 8%, compared with 13 +/- 2% in controls. Na-K-ATPase activity per millimeter tubule length increased by 225% in the cortical collecting tubule and by 177% in the medullary collecting tubule, but was not substantially affected in other nephron segments. Stimulation of Na-K-ATPase was identical in the cortical collecting tubule of K-loaded mice treated with spironolactone. These results indicate that chronic potassium loading in the mouse results in an adaptive increase potassium loading in the mouse results in an adaptive increase in Na-K-ATPase in the collecting tubule and suggest that this nephron segment is the major site of potassium adaptation in this species. This effect appears to be independent of aldosterone.

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