Properties of the basolateral membrane of the cortical thick ascending limb of Henle's loop of rabbit kidney

1983 ◽  
Vol 396 (4) ◽  
pp. 325-334 ◽  
Author(s):  
Rainer Greger ◽  
Eberhard Schlatter
Keyword(s):  
Basolateral Membrane ◽  
Rabbit Kidney ◽  
Thick Ascending Limb ◽  
Henle's Loop

Characterization of Aldose Reductase from the Thick Ascending Limb of Henle’s Loop of Rabbit Kidney

Nephron ◽  
2001 ◽  
Vol 89 (1) ◽  
pp. 73-81 ◽  
Author(s):  
R. Willi Grunewald ◽  
Angela Eckstein ◽  
Claudius H. Reisse ◽  
Gerhard A. Müller
Keyword(s):  
Aldose Reductase ◽  
Rabbit Kidney ◽  
Thick Ascending Limb ◽  
Henle's Loop

Characterization of basolateral chloride/bicarbonate exchange in macula densa cells

2005 ◽  
Vol 288 (2) ◽  
pp. F380-F386 ◽  
Author(s):  
Peter Komlosi ◽  
Sebastian Frische ◽  
Amanda L. Fuson ◽  
Attila Fintha ◽  
Ákos Zsembery ◽  
...  
Keyword(s):  
Anion Exchange ◽  
Basolateral Membrane ◽  
Macula Densa ◽  
Rabbit Kidney ◽  
Thick Ascending Limb ◽  
Nacl Concentration ◽  
High Concentrations ◽  
Immunohistochemical Studies ◽  
Exchange Activity

Functional and immunohistological studies were performed to identify basolateral chloride/bicarbonate exchange in macula densa cells. Using the isolated, perfused thick ascending limb with attached glomerulus preparation dissected from rabbit kidney, macula densa intracellular pH (pHi) was measured with fluorescence microscopy and BCECF. For these experiments, basolateral chloride was reduced, resulting in reversible macula densa cell alkalinization. Anion exchange activity was assessed by measuring the maximal net base efflux on readdition of bath chloride. Anion exchange activity required the presence of bicarbonate, was independent of changes in membrane potential, did not require the presence of sodium, and was inhibited by high concentrations of DIDS. Inhibition of macula densa anion exchange activity by basolateral DIDS increased luminal NaCl concentration-induced elevations in pHi. Immunohistochemical studies using antibodies against AE2 demonstrated expression of AE2 along the basolateral membrane of macula densa cells of rabbit kidney. These results suggest that macula densa cells functionally and immunologically express a chloride/bicarbonate exchanger at the basolateral membrane. This transporter likely participates in the regulation of pHi and might be involved in macula densa signaling.

Cytosolic [Ca2+] signaling pathway in macula densa cells

1999 ◽  
Vol 277 (3) ◽  
pp. F472-F476 ◽  
Author(s):  
János Peti-Peterdi ◽  
P. Darwin Bell
Keyword(s):  
Signaling Pathway ◽  
Basolateral Membrane ◽  
Chloride Concentration ◽  
Cytosolic Calcium ◽  
Inhibitory Effect ◽  
Macula Densa ◽  
Rabbit Kidney ◽  
Bathing Solution ◽  
Thick Ascending Limb ◽  
Voltage Gated

Previous micropuncture studies suggested that macula densa (MD) cells might detect variations in luminal sodium chloride concentration ([NaCl]l) through changes in cytosolic calcium ([Ca2+]c). To test this hypothesis, MD [Ca2+]cwas measured with fluorescence microscopy using fura 2 in the isolated perfused thick ascending limb with attached glomerulus preparation dissected from rabbit kidney. Tubules were bathed and perfused with a Ringer solution, [NaCl]l was varied and isosmotically replaced with N-methyl-d-glucamine cyclamate. Control [Ca2+]c, during perfusion with 25 mM NaCl and 150 mM NaCl in the bath, averaged 101.6 ± 8.2 nM ( n = 21). Increasing [NaCl]l to 150 mM elevated [Ca2+]cby 39.1 ± 5.2 nM ( n = 21, P < 0.01). This effect was concentration dependent between zero and 60 mM [NaCl]l. The presence of either luminal furosemide or basolateral nifedipine or 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB), a potent Cl− channel blocker, significantly reduced resting [Ca2+]cand abolished the increase in [Ca2+]cin response to increased [NaCl]l. Nifedipine failed to produce a similar inhibitory effect when added exclusively to the luminal perfusate. Also, 100 nM BAY K 8644, a voltage-gated Ca2+ channel agonist, added to the bathing solution increased [Ca2+]cby 33.2 ± 8.1 nM ( n = 5, P < 0.05). These observations suggest that MD cells may detect variations in [NaCl]l through a signaling pathway that includes Na+-2Cl−-K+cotransport, basolateral membrane depolarization via Cl− channels, and Ca2+ entry through voltage-gated Ca2+ channels.

Cl− channels in basolateral renal medullary membranes XII. Anti-rbClC-Ka antibody blocks MTAL Cl−channels

1997 ◽  
Vol 273 (6) ◽  
pp. F1030-F1038 ◽  
Author(s):  
Christopher J. Winters ◽  
Ludwika Zimniak ◽  
W. Brian Reeves ◽  
Thomas E. Andreoli
Keyword(s):  
Lipid Bilayers ◽  
Collecting Duct ◽  
Basolateral Membrane ◽  
Rabbit Kidney ◽  
Thick Ascending Limb ◽  
Cortical Collecting Duct ◽  
Patch Clamp Technique ◽  
Medullary Thick Ascending Limb ◽  
Acid Fragment ◽  
Cl Channels

Cl− channels in the medullary thick ascending limb (MTAL) studied by either patch-clamp technique or reconstitution into lipid bilayers are activated by increases in intracellular Cl−concentrations. rbClC-Ka, a ClC Cl− channel, may represent this channel. We therefore evaluated the role of rbClC-Ka in transcellular MTAL Cl− transport in two separate ways. First, an antibody was raised against a fusion protein containing a 153-amino acid fragment of rbClC-Ka. Immunostaining of rabbit kidney sections with the antibody was localized to basolateral regions of MTAL and cortical thick ascending limb (CTAL) segments and also to the cytoplasm of intercalated cells in the cortical collecting duct. Second, Cl− uptake and efflux were measured in suspensions of mouse MTAL segments. Cl− uptake was bumetanide sensitive and was stimulated by treatment with a combination of vasopressin + forskolin + dibutyryl adenosine 3′,5-cyclic monophosphate (DBcAMP). Cl− efflux was also increased significantly by vasopressin + forskolin + DBcAMP from 114 ± 20 to 196 ± 36 nmol ⋅ mg protein−1 ⋅ 45 s−1( P = 0.003). Cl− efflux was inhibited by the Cl− channel blocker diphenylamine-2-carboxylate (154 ± 26 vs. 70 ± 21 nmol ⋅ mg protein−1 ⋅ 45 s−1, P = 0.003). An anti-rbClC-Ka antibody, which inhibits the activity of MTAL Cl− channels in lipid bilayers, reduced Cl− efflux from intact MTAL segments (154 ± 28 vs. 53 ± 14 nmol ⋅ mg protein−1 ⋅ 45 s−1, P = 0.02). These results support the view that rbClC-Ka is the basolateral membrane Cl− channel that mediates vasopressin-stimulated net Cl− transport in the MTAL segment.

A potassium channel in the apical membrane of rabbit thick ascending limb of Henle's loop

1990 ◽  
Vol 258 (2) ◽  
pp. F244-F253 ◽  
Author(s):  
W. H. Wang ◽  
S. White ◽  
J. Geibel ◽  
G. Giebisch
Keyword(s):  
Apical Membrane ◽  
Rabbit Kidney ◽  
K Channel ◽  
Thick Ascending Limb ◽  
Dependent Manner ◽  
Patch Clamp Technique ◽  
Bath Solution ◽  
Henle's Loop ◽  
Voltage Dependent ◽  
Inside Out

We used the patch-clamp technique to study the activity of single potassium channels in the apical membrane of isolated thick ascending limbs of Henle's loop (TAL) of rabbit kidneys. In cell-attached patches with NaCl Ringer or high-K+ solution in the bath and 140 mM K+ in the pipette, an inwardly rectifying K+ channel was observed with an inward slope conductance of 22.0 +/- 0.5 pS and outward slope conductance of 10.2 +/- 0.3 pS at 22 degrees C (n = 15). The channel was highly selective for K+, with a calculated permeability ratio for K(+)-to-Na+ of 20:1 (n = 4). The open probability (Po) of the channel was 0.89 +/- 0.03 (n = 15) and was not voltage dependent. In inside-out patches with 140 mM K+ in both the bath and the pipette solutions, both Po and conductance of the channel were similar to that in cell-attached patches. Addition of 0.1 mM Ba2+ to the pipette solution reduced Po of the channel in a voltage-dependent manner. Lowering the pH of the bath solution from 7.4 to 6.9 or increasing Ca2+ concentration from 0 to 0.5 mM in inside-out patches did not alter either Po or conductance of the channel. Addition of 2 mM ATP to the bath solution completely inhibited channel activity. This ATP-induced inhibition was fully reversible and was found to be dependent on the ratio of ATP to ADP, since adding 1 mM ADP to the bath solution relieved the ATP-induced blockade. The property of this small-conductance K+ channel make it a likely candidate for recycling of K+ across the apical membrane of TAL of the rabbit kidney. ATP and ADP are possible intracellular regulators of the channel's activity.

Insulin stimulates NaCl transport in isolated perfused MTAL of Henle's loop of rabbit kidney

1994 ◽  
Vol 267 (2) ◽  
pp. F265-F270 ◽  
Author(s):  
O. Ito ◽  
Y. Kondo ◽  
N. Takahashi ◽  
K. Kudo ◽  
Y. Igarashi ◽  
...  
Keyword(s):  
Kinase Inhibitor ◽  
Basolateral Membrane ◽  
Rabbit Kidney ◽  
Thick Ascending Limb ◽  
Maximal Effect ◽  
Nacl Transport ◽  
Luminal Membrane ◽  
Camp Analogue

To elucidate the mechanism of Na+ retention by insulin in vivo, the direct tubular effect of insulin on NaCl transport in the in vitro microperfused medullary thick ascending limb of Henle (MTAL) was examined. Insulin at 10(-6) mol/l in the bath increased transepithelial voltage (Vte) from 3.1 +/- 0.3 to 5.7 +/- 0.3 mV (n = 12, P < 0.0001). The effect of insulin on Vte was dependent on its concentration, and the half-maximal effect of insulin was observed at 5 x 10(-9) mol/l. Insulin at 10(-6) mol/l also caused a significant decrease of luminal Cl- concentration from 85.4 +/- 5.0 to 62.8 +/- 3.0 mmol/l (n = 5, P < 0.002) when the lumen was microperfused constantly at less than 1 nl/min. Insulin at 10(-6) mol/l also increased net lumen-to-bath Cl- flux (JCl) from 143 +/- 15 to 292 +/- 37 pmol.mm-1.min-1 (n = 5, P < 0.004). When the Na(+)-K(+)-adenosinetriphosphatase (Na(+)-K(+)-ATPase) in the basolateral membrane was blocked by 10(-4) mol/l ouabain, the insulin-mediated increase in Vte was completely suppressed. When the Na(+)-K(+)-2Cl- cotransporter in the luminal membrane of the MTAL was blocked by 10(-4) mol/l furosemide, the insulin-mediated increase in Vte was also abolished. To test whether adenosine 3',5'-cyclic monophosphate (cAMP) contributes to the action of insulin, we examined the effect of cAMP analogue and cAMP-dependent protein kinase inhibitor on the action of insulin. A maximal concentration (5 x 10(-4) mol/l) of dibutyryl-cAMP (DBcAMP) increased Vte and JCl.(ABSTRACT TRUNCATED AT 250 WORDS)

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