The effect of cyanide on apparent potassium conductance across the peritubular cell membrane of frog proximal tubules

1986 ◽  
Vol 407 (6) ◽  
pp. 607-610 ◽  
Author(s):  
W. Rehwald ◽  
F. Lang
Keyword(s):  
Cell Membrane ◽  
Potassium Conductance ◽  
Proximal Tubules

The collecting tubule of Amphiuma. I. Electrophysiological characterization

1987 ◽  
Vol 253 (6) ◽  
pp. F1263-F1272 ◽  
Author(s):  
M. Hunter ◽  
J. D. Horisberger ◽  
B. Stanton ◽  
G. Giebisch
Keyword(s):  
Cell Membrane ◽  
Cell Model ◽  
Basolateral Membrane ◽  
Apical Cell ◽  
Potassium Conductance ◽  
Sodium Reabsorption ◽  
Apical Cell Membrane ◽  
Cation Selectivity ◽  
Basolateral Cell Membrane ◽  
Collecting Tubules

Single collecting tubules of Amphiuma kidneys were perfused in vitro to characterize their electrophysiological properties. The lumen-negative potential (-24 mV) was abolished by amiloride in the lumen and by ouabain in the bath. Ion substitution experiments in the lumen demonstrated the presence of a large sodium conductance in the apical cell membrane, but no evidence was obtained for a significant potassium or chloride conductance. Ion substitutions in the bath solution and the depolarizing effect of barium on the basolateral membrane potential demonstrated the presence of a large potassium conductance in the basolateral cell membrane. Measurements of dilution potentials in amiloride-treated tubules revealed a modest cation selectivity of the paracellular pathway. These results support a cell model in which sodium reabsorption occurs by electrodiffusion across the apical cell membrane and active transport across the basolateral cell membrane. The absence of a detectable potassium conductance in the apical cell membrane suggests that secretion of this ion cannot take place by diffusion from cell to lumen.

Regulation of cytosolic free calcium in isolated perfused proximal tubules of Necturus

1988 ◽  
Vol 255 (4) ◽  
pp. F787-F799
Author(s):  
J. M. Yang ◽  
C. O. Lee ◽  
E. E. Windhager
Keyword(s):  
Cell Membrane ◽  
Control Level ◽  
Potential Gradient ◽  
Cytosolic Calcium ◽  
Ringer Solution ◽  
Proximal Tubules ◽  
Free Calcium ◽  
Ion Activity ◽  
Renal Tubular Transport ◽  
Renal Tubular

To study the role of intracellular Ca2+ in regulating renal tubular transport of ions and water, cytosolic calcium ion activity (aiCa), cytosolic sodium ion activity (aiNa), and intracellular pH (pHi) in cells of isolated perfused proximal tubules of Necturus kidney were measured with Ca2+-, Na+-, and H+-selective microelectrodes, respectively. In control conditions, i.e., HCO3-Ringer solution on both sides of the epithelium, aiCa was 82 +/- 7 (SE) nM (n = 54), aiNa averaged 12.8 +/- 0.4 mM (n = 53), and pHi was 7.33 +/- 0.03 (n = 27). When the Na-K pump was inhibited by nominally K-free Ringer circumfusion, aiCa increased from a control level of 75 +/- 13 to 237 +/- 40 nM (paired t test; n = 16; P less than 0.001); in a different set of tubules, aiNa rose from 11.3 +/- 0.6 to 51.5 +/- 5.8 mM (n = 11; P less than 0.001). When organic solutes were deleted in the luminal perfusate, aiCa decreased from 73 +/- 11 to 61 +/- 11 nM (n = 9; P less than 0.001) and aiNa decreased from 14.6 +/- 0.6 to 8.3 +/- 0.7 mM (n = 9; P less than 0.001). Depolarization of the peritubular cell membrane with high-K, low-Na Ringer decreased aiCa from 90 +/- 12 to 55 +/- 9 nM (n = 13; P less than 0.001) and reduced aiNa from 13.1 +/- 1.0 to 7.5 +/- 0.6 mM (n = 16; P less than 0.001). Ionomycin (2 X 10(-6) M) increased aiCa from 67 +/- 10 to 158 +/- 26 nM (n = 10; P less than 0.001) and pHi from 7.33 +/- 0.03 to 7.39 +/- 0.03 (n = 27; P less than 0.001) but reduced aiNa from 11.8 +/- 0.9 to 10.3 +/- 0.7 mM (n = 11; P less than 0.001). The data are consistent with the view that aiCa is determined, in part, by the magnitude of the electrochemical potential gradient for Na ions across the basolateral cell membrane.

Amiloride reduces potassium conductance in frog kidney via inhibition of Na+-H+ exchange

1986 ◽  
Vol 251 (1) ◽  
pp. F66-F73
Author(s):  
H. Oberleithner ◽  
G. Munich ◽  
A. Schwab ◽  
P. Dietl
Keyword(s):  
Cell Membrane ◽  
Potassium Conductance ◽  
Membrane Resistance ◽  
Frog Kidney ◽  
High Potassium ◽  
Diluting Segment ◽  
Nephron Segment ◽  
Net Flux ◽  
Kidney Perfusion ◽  
K Concentration

The existence of a carrier-mediated Na+-H+ exchange has been described recently in many epithelial and nonepithelial tissues including the diluting segment of the amphibian kidney. In this preparation the Na+-H+ exchanger is dramatically stimulated by so-called K+ adaptation (chronic exposure of animals to high potassium) and completely inhibited by the diuretic drug amiloride. We performed electrophysiological experiments in diluting segments of the isolated perfused frog kidney to investigate whether amiloride affects the conductance properties of this epithelium. Amiloride dramatically increased the transepithelial resistance and the ratio of lumen over peritubular cell membrane resistance. Cell membrane potential changes, induced by luminal K+ concentration steps, were blunted by luminal application of amiloride, by luminal Na+-free perfusates, or by acidification of the kidney perfusion solution. K+ secretory net flux, measured by K+-sensitive microelectrodes, decreased by half in presence of the diuretic. The experiments reveal that amiloride reduces the K+ conductance of the luminal cell membrane of frog diluting segment via inhibition of the luminal Na+-H+ exchanger. This decreases transepithelial K+ net secretion in this nephron segment.

Progesterone inhibits K conductance in plasma membrane of cultured renal epitheloid MDCK cells

1991 ◽  
Vol 260 (5) ◽  
pp. E743-E750 ◽  
Author(s):  
M. Steidl ◽  
G. Pinggera ◽  
M. Ritter ◽  
F. Lang
Keyword(s):  
Cell Membrane ◽  
Channel Blocker ◽  
Mdck Cells ◽  
Extracellular Fluid ◽  
Potassium Conductance ◽  
Membrane Resistance ◽  
Acute Administration ◽  
Madin Darby Canine Kidney ◽  
Ru 486 ◽  
Darby Canine Kidney

Progesterone causes natriuresis, an effect largely attributed to displacement of aldosterone from its receptor. The present study, however, demonstrates that progesterone (0.1, 1, and 10 mumol/1, respectively) also causes a rapid, fully reversible depolarization of Madin-Darby canine kidney (MDCK) cells (by 1.3 +/- 0.5, 4.1 +/- 0.7 and 12.3 +/- 1.5 mV, respectively). 17 alpha-Hydroxyprogesterone and dihydroxytestosterone are, by two orders of magnitude, less effective, whereas cholesterol, aldosterone, hydrocortisone, and estradiol (each up to 10 mumol/l) did not significantly alter the potential difference across the cell membrane. The effect of progesterone is blunted by antiprogestogen RU 486 (5 mumol/l). The progesterone-induced depolarization is paralleled by a decrease of potassium selectivity and an increase of cell membrane resistance and is abolished in the presence of the potassium channel blocker barium (10 mmol/l), as well as in the presence of 40 mmol/l potassium in the extracellular fluid. Neither removal of extracellular chloride or bicarbonate nor amiloride, ouabain, or pretreatment with pertussis toxin abolish the depolarizing effect of 5 mumol/l progesterone. In conclusion, acute administration of progesterone depolarizes MDCK cells by decreasing the potassium conductance of the cell membrane.

Activation of cell membrane potassium conductance by mercury in cultured renal epitheloid (MDCK) cells

1991 ◽  
Vol 146 (1) ◽  
pp. 25-33 ◽  
Author(s):  
A. Jungwirth ◽  
M. Ritter ◽  
M. Paulmichl ◽  
F. Lang
Keyword(s):  
Cell Membrane ◽  
Mdck Cells ◽  
Potassium Conductance
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