Effects of acid base disturbances on basolateral membrane potential and intracellular potassium activity in the proximal tubule ofNecturus

1983 ◽  
Vol 73 (1) ◽  
pp. 61-68 ◽  
Author(s):  
Takahiro Kubota ◽  
Bruce A. Biagi ◽  
Gerhard Giebisch
Keyword(s):  
Membrane Potential ◽  
Proximal Tubule ◽  
Basolateral Membrane ◽  
Acid Base ◽  
Intracellular Potassium ◽  
Intracellular Potassium Activity ◽  
Basolateral Membrane Potential

Adaptive responses to Na(+)-coupled solute transport and osmotic cell swelling in salamander proximal tubule

1994 ◽  
Vol 267 (3) ◽  
pp. F479-F488
Author(s):  
S. W. Weinstein ◽  
C. Clausen
Keyword(s):  
Membrane Potential ◽  
Proximal Tubule ◽  
Adaptive Response ◽  
Basolateral Membrane ◽  
Proximal Tubules ◽  
Cell Swelling ◽  
Adaptive Responses ◽  
High Concentration ◽  
Luminal Perfusion ◽  
Basolateral Membrane Potential

Measurements of basolateral membrane potential and relative K+ conductance were performed in isolated perfused proximal tubules from Ambystoma. To investigate adaptive increases in basolateral membrane K+ conductance (gK) associated with Na(+)-solute cotransport, measurements were made comparing transport of glucose and alanine, with changes caused by hypotonicity- and solute-induced cell swelling. Luminal perfusion with alanine produced results consistent with an adaptive increase in gK; perfusion with glucose failed to show this response. Hypotonic peritubular solutions also produced results consistent with an adaptive increase in gK, but isosmotic increases of peritubular glucose sufficient to swell the cells failed to produce this. No changes in the responses to luminal perfusion with alanine or glucose were induced by hypotonic peritubular solutions. With a high concentration of glucose in isosmotic peritubular solutions, perfusion of the lumen with glucose now produced results consistent with an adaptive increase in gK. Isosmotic peritubular solutions containing urea produced adaptive changes similar to those observed using hypotonic peritubular solutions, but when glucose was subsequently added to the lumen, no further adaptive response occurred. We conclude that cell swelling alone is insufficient to explain the mechanisms involved in the adaptive responses of gK occurring during Na(+)-solute cotransport in the salamander proximal tubule.

Effect of norepinephrine on intracellular pH in kidney proximal tubule: role of Na+-( HCO 3 − ) n cotransport

1998 ◽  
Vol 275 (1) ◽  
pp. F33-F45 ◽  
Author(s):  
Solange Abdulnour-Nakhoul ◽  
Raja N. Khuri ◽  
Nazih L. Nakhoul
Keyword(s):  
Membrane Potential ◽  
Proximal Tubule ◽  
Intracellular Ph ◽  
Basolateral Membrane ◽  
Inhibitory Effect ◽  
Rate Of Change ◽  
Kidney Proximal Tubule ◽  
Luminal Membrane ◽  
Basolateral Membrane Potential

We examined the effect of norepinephrine (NE) on intracellular pH (pHi) and activity of Na+([Formula: see text]) in the isolated perfused kidney proximal tubule of Ambystoma, using single-barreled voltage and ion-selective microelectrodes. In control[Formula: see text] Ringer, addition of 10−6 M NE to the bath reversibly depolarized the basolateral membrane potential ( V 1), the luminal membrane potential ( V 2), and the transepithelial potential difference ( V 3) and increased pHi by 0.14 ± 0.02. These effects were mimicked by isoproterenol but were abolished after pretreatment with SITS or in the absence of CO2/[Formula: see text]. Removal of bath Na+ depolarized V 1 and V 2, hyperpolarized V 3, and decreased pHi. These effects are largely mediated by the electrogenic Na+-([Formula: see text]) n cotransporter. In the presence of NE, the effects of Na+ removal on membrane potential differences and the rate of change of pHi were significantly smaller. Reducing bath [Formula: see text] concentration from 10 to 2 mM at constant CO2 (pH 6.8) depolarized V 1 and V 2, decreased pHi, and lowered[Formula: see text]. These changes are also due to Na+-([Formula: see text]) n . In the presence of NE, reducing bath [[Formula: see text]] caused a smaller depolarizations of V 1 and V 2, and the rate of pHi decrease was significantly reduced. Our results indicate: 1) NE causes an increase in pHi; 2) the NE-induced alkalinization is mediated by a SITS-sensitive and[Formula: see text]-dependent transporter on the basolateral membrane; and 3) in the presence of NE, the reduced effects caused by basolateral[Formula: see text] changes or Na+ removal are indicative of an inhibitory effect of NE on Na+-([Formula: see text]) n cotransport.

Electrophysiology of salamander proximal tubule. I. Effects of rapid cooling

1986 ◽  
Vol 251 (2) ◽  
pp. F319-F333
Author(s):  
H. Sackin
Keyword(s):  
Membrane Potential ◽  
Low Temperature ◽  
Proximal Tubule ◽  
Basolateral Membrane ◽  
Bath Temperature ◽  
Ambystoma Tigrinum ◽  
Ionic Selectivity ◽  
Anion Selectivity ◽  
Nacl Concentration ◽  
Basolateral Membrane Potential

The response of the amphibian proximal tubule to a rapid decrease in temperature was studied in isolated perfused tubules of Ambystoma tigrinum. Cooling from 23 to 4 degrees C increased paracellular and cellular electrical resistances by factors of 1.7 and 3.6, respectively, but had virtually no effect on the ionic selectivity of the paracellular pathway. When lumen and bath solutions were maintained identical by rapid tubule perfusion, decreasing bath temperature from 22 to 0 degree C in 400 ms depolarized the transepithelial potential (Vte) from -3.7 +/- 0.3 to -1.1 +/- 0.2 mV and depolarized the basolateral membrane potential (Vbl) from -52 +/- 3 to -45 +/- 3 mV (n = 12). These fast depolarizations were followed by slower depolarizations of both Vte and Vbl that continued throughout the period of low temperature. Only approximately 30% of the initial slow depolarization of Vte at low temperature could be explained by changes in electrical resistance and cell membrane potential. The remaining 70% of this Vte depolarization at low temperature is consistent with equilibration of a hypertonic interspace with isotonic lumen and bath solutions. Given the anion selectivity of Ambystoma proximal tubule, the magnitude of this slow Vte depolarization implies an interspace NaCl concentration 2-5% higher than the NaCl concentration in either the lumen or bath solutions.

Succinate alters respiration, membrane potential, and intracellular K+ in proximal tubule

1988 ◽  
Vol 255 (6) ◽  
pp. F1170-F1177 ◽  
Author(s):  
S. R. Gullans ◽  
B. C. Kone ◽  
M. J. Avison ◽  
G. Giebisch
Keyword(s):  
Membrane Potential ◽  
Atpase Activity ◽  
Ion Transport ◽  
Proximal Tubule ◽  
Basolateral Membrane ◽  
Coupling Efficiency ◽  
Atp Synthesis ◽  
Dependent Manner ◽  
Kinetic Evaluation ◽  
Apparent Increase

Succinate, a dicarboxylic acid, is an intermediate in the Krebs cycle that is transported and metabolized by the renal proximal tubule. It is also known to increase proximal tubule transport of phosphate and glucose but not fluid by unknown mechanisms. In the present study, succinate increased proximal tubule respiration in a dose-dependent manner, and a kinetic evaluation indicated that two separate processes were activated. A lower-affinity (Km = 0.9 mM), higher-capacity stimulation (Vmax increase of 49%) was attributed to a decrease in the mitochondrial coupling efficiency. A higher-affinity process (Km = 0.012 mM) was related to an apparent increase in ATP synthesis. The apparent increase in ATP synthesis was not associated with a change in Na+-K+-ATPase activity, however, but rather indicated a 49% increase in ion transport-independent ATP utilization. Basolateral membrane potential hyperpolarized by -7 mV in the presence of succinate, and this was related to an increase in the K+ transference number. Finally, 1 and 5 mM succinate promoted a net cellular uptake of K+, leading to an 11% increase in intracellular K+, which was not the result of an increase in Na+-K+-ATPase activity. Thus the cellular entry and metabolism of succinate promotes multiple changes in ion transport without altering Na+-K+-ATPase activity.

Intracellular potassium activities in Amphiuma small intestine

1976 ◽  
Vol 231 (4) ◽  
pp. 1214-1219 ◽  
Author(s):  
JF White
Keyword(s):  
Small Intestine ◽  
Membrane Potential ◽  
Activity Coefficient ◽  
Potassium Concentration ◽  
Equilibrium Potential ◽  
Absorptive Cell ◽  
Buffer Solution ◽  
Intracellular Potassium ◽  
Intracellular Potassium Activity ◽  
Liquid Ion Exchanger

Intracellular potassium activity (aKi) has been determined in absorptive cells lining the villi of isolated, stripped proximal segments of Amphiuma small intestine. With single-barreled liquid ion-exchanger microelectrodes aKi = 41.6 +/- 1.5 mM in normal chloride buffer; with double-barreled microelectrodes constructed by a new method aKi = 38.5 +/- 2.4 mM. Also, by the latter approach aKi = 41.1 +/- 2.1 mM in buffer in which potassium was elevated to 5 meq/liter and aKi = 44.2 +/- 1.3 mM in sulfate buffer with the same bath potassium concentration. Since the calculated potassium equilibrium potential exceeds the membrane potential this ion is accumulated by the intestinal absorptive cell. A major portion of cellular potassium is bound or compartmentalized since the intracellular potassium activity coefficient is very low. A layer exists near the villi in which the potassium activity exceeds that in the bath buffer solution.

Relation of membrane potential to basolateral TEA transport in isolated snake proximal renal tubules

1995 ◽  
Vol 268 (6) ◽  
pp. R1539-R1545 ◽  
Author(s):  
Y. K. Kim ◽  
W. H. Dantzler
Keyword(s):  
Steady State ◽  
Membrane Potential ◽  
Potent Inhibitor ◽  
Basolateral Membrane ◽  
Potential Difference ◽  
Renal Tubules ◽  
K Concentration ◽  
Electrochemical Equilibrium ◽  
Membrane Potential Difference ◽  
Basolateral Membrane Potential

We measured the effects of changes in bath K+ concentration ([K+]) on basolateral membrane potential difference (PD) and [3H]tetraethylammonium (TEA) transport in isolated snake (Thamnophis) proximal renal tubules (25 degrees C; pH 7.4). Increasing bath [K+] from 3 to 65 mM decreased PD from -60 mV (inside of cells negative) to -20 mV and 2-min uptake of [3H]TEA by approximately 25%, indicating that PD influences TEA entry into the cells. Uptake of [3H]TEA was inhibited similarly at both K+ concentrations by unlabeled TEA, indicating that uptake is carrier mediated. Kt (approximately 18 microM) for 2-min uptake of [3H]TEA in 3 mM K+ increased significantly in 65 mM K+, suggesting that the decrease in PD or the increase in [K+] alters the affinity of the transporter for TEA. The steady-state cell-to-bath ratio for [3H]TEA with 3 mM K+ (-60 mV PD) was approximately 16, significantly above the ratio of 10 predicted for passive distribution at electrochemical equilibrium. With 65 mM K+ (-20 mV PD) this ratio decreased to approximately 6, again significantly above the predicted ratio of 2. These data suggest that the PD can account for much, but not all, of the steady-state uptake of TEA. Efflux of [3H]TEA across the basolateral membrane was identical with either 3 or 65 mM K+ in the bath but was almost completely inhibited in either case by tetrapentylammonium, a potent inhibitor of TEA uptake. These data indicate that virtually all TEA transport across the basolateral membrane is carrier mediated and that transport out of the cells is unaffected by PD.

Intracellular potentials in rabbit proximal tubules perfused in vitro

1981 ◽  
Vol 240 (3) ◽  
pp. F200-F210 ◽  
Author(s):  
B. Biagi ◽  
T. Kubota ◽  
M. Sohtell ◽  
G. Giebisch
Keyword(s):  
Membrane Potential ◽  
Basolateral Membrane ◽  
Proximal Tubules ◽  
Rabbit Kidney ◽  
Electrical Measurements ◽  
Proximal Tubular ◽  
The Mean ◽  
Number Of Cells ◽  
Basolateral Membrane Potential

Conventional microelectrodes were used to measure the basolateral membrane potential (VBL) in isolated perfused superficial proximal convoluted (sPCT) and superficial proximal straight (sPST) tubules of the rabbit kidney. Stable recordings for periods up to 2 h can be obtained. The mean +/- SE (n = number of cells) values of VBL were sPCT = -51.0 +/- 1.63 (24) and sPST = -47.0 +/- 0.97 (94) mV. Inhibitors of active transport, ouabain (10(-5) M) and low bath potassium (0.1 mM), caused a significant depolarization of VBL in sPST. In contrast, short-duration bath cooling (10 degrees C) had no significant effect. Removal of luminal glucose caused a larger hyperpolarization in sPCT (-13.9 +/- 1.77 (9) mV) than in sPST (-3.8 +/- 1.02 (5) mV). Removal of luminal glucose and alanine resulted in an even larger hyperpolarization of VBL in sPCT (-19.0 +/- 0.44 (6) mV). Perfusion of the lumen with a solution resembling late proximal tubular fluid in sPST resulted in hyperpolarization of VBL (-4.3 +/- 0.85 (4) mV). Reducing bath pH to 6.7 depolarized VBL (39.9 +/- 1.77 (13) mV). This effect can be associated with a decrease in the relative potassium permeability of the basolateral membrane. These results demonstrate the feasibility of using intracellular electrical measurements to determine both luminal and basolateral membrane characteristics in isolated proximal tubular segments.

Direct measurement of basolateral membrane potentials from cells of the macula densa

1989 ◽  
Vol 257 (3) ◽  
pp. F463-F468 ◽  
Author(s):  
P. D. Bell ◽  
J. Y. Lapointe ◽  
J. Cardinal
Keyword(s):  
Membrane Potential ◽  
Direct Measurement ◽  
Basolateral Membrane ◽  
Membrane Potentials ◽  
Macula Densa ◽  
Rabbit Kidney ◽  
Fluid Composition ◽  
Nacl Solution ◽  
Basolateral Membrane Potential

At the present time, little is known concerning the electrophysiology of the cells of the macula densa and whether or not these cells are electrically responsive to alterations in luminal fluid composition. To investigate this issue, cortical thick ascending limbs (CTAL) containing macula densa and attached glomeruli were dissected from rabbit kidney and the CTAL perfused in vitro. Basolateral membrane potential (Vbl) was measured with microelectrodes in macula densa cells and, for comparison, in cells of the CTAL. Macula densa Vbl averaged -56.5 +/- 7.6 mV (n = 4) at a (n = 22) at 20 mM NaCl, -35.6 +/- 3.9 mV (n = 16) at 45 mM NaCl, and -25.5 +/- 2.6 mV (n = 32) at 150 mm NaCl. Thus macula densa Vbl depolarized markedly (31 mV) when luminal perfusate [NaCl] was increased from low to high values. In contrast, Vbl measured in CTAL cells averaged -62 +/- 6.1 mV (n = 6) in 45 mM NaCl and did not change significantly as perfusate NaCl was increased to 150 mM. In the presence of 150 mM NaCl, luminal application of furosemide (50 microM) produced a small (3.5 +/- 1.1 mV, n = 16) but statistically significant (P less than 0.02) hyperpolarization in macula densa cells, whereas CTAL cell Vbl hyperpolarized markedly (20 +/- 5.7 mV, n = 6) with addition of furosemide. Finally, neither macula densa cells nor the CTAL cells changed Vbl when 45 mM NaCl solution was made hypotonic by removing mannitol.(ABSTRACT TRUNCATED AT 250 WORDS)

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