Effects of inhibitors and ion substitutions on oscillations of cell membrane potential in cells expressing the RAS oncogene

1992 ◽  
Vol 421 (5) ◽  
pp. 416-424 ◽  
Author(s):  
F. Lang ◽  
S. Waldegger ◽  
E. Woell ◽  
M. Ritter ◽  
K. Maly ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Cell Membrane ◽  
Cell Membrane Potential ◽  
Ras Oncogene ◽  
In Cells

scholarly journals Bradykinin-induced oscillations of cell membrane potential in cells expressing the Ha-ras oncogene.

1991 ◽  
Vol 266 (8) ◽  
pp. 4938-4942
Author(s):  
F Lang ◽  
F Friedrich ◽  
E Kahn ◽  
E Wöll ◽  
M Hammerer ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Cell Membrane ◽  
Cell Membrane Potential ◽  
Ras Oncogene ◽  
In Cells

scholarly journals Intracellular pH regulation in freshly isolated suspensions of rabbit inner medullary collecting duct cells: role of Na+:H+ antiporter and H(+)-ATPase.

1990 ◽  
Vol 1 (6) ◽  
pp. 890-901
Author(s):  
D Kikeri ◽  
M L Zeidel
Keyword(s):  
Membrane Potential ◽  
Cell Membrane ◽  
Intracellular Ph ◽  
Recovery Rate ◽  
Collecting Duct ◽  
Atp Depletion ◽  
Cell Membrane Potential ◽  
Inner Medullary Collecting Duct ◽  
Medullary Collecting Duct ◽  
In Cells

To define proton transport mechanisms involved in the regulation of intracellular pH (pHi) in cells of the inner medullary collecting duct (IMCD), pHi and cell membrane potential were estimated by using the fluorescent dyes 2,7-biscarboxyethyl-5(6)-carboxyfluorescein and 3,3'-dipropylthiadicarbocyanine iodide, respectively, in suspensions of freshly isolated rabbit IMCD cells. The resting pHi of IMCD cells in nonbicarbonate Ringer's solution (pH 7.4) was 7.21 +/- 0.03 (mean +/- SE). When cells were acidified by ammonium withdrawal, the initial pHi recovery rate was 0.33 +/- 0.02 pH unit/min; replacement of extracellular Na+ (130 mM) with N-methyl-D-glucamine+ reduced the pHi recovery rate to 0.08 +/- 0.02 pH unit/min, while addition of 0.1 mM amiloride in the presence of extracellular Na+ reduced the rate of pHi recovery to 0.02 +/- 0.02 pH unit/min. Similar results were obtained in cells acid loaded with HCl. Cells recovering from acidification exhibited 22Na+ uptake rates threefold higher than did nonacidified cells. The rate of Na(+)-dependent pHi recovery was independent of the cell membrane potential. In the absence of extracellular Na+, depolarizing cell membrane potential in a stepwise manner by increasing extracellular K+ concentrations from 1 to 130 mM resulted in graded increments in the rate of pHi recovery. In the presence of 130 mM K+, the pHi recovery rate in acidified cells was dependent on cellular ATP levels, sensitive to 1 mM N-ethylmaleimide, and insensitive to 0.01 mM oligomycin in the presence of glucose (control, 0.24 +/- 0.01; ATP-depleted, 0.13 +/- 0.02; addition of N-ethylmaleimide, 0.16 +/- 0.01; addition of oligomycin, 0.27 +/- 0.02 pH unit/min). ATP depletion markedly inhibited H+ extrusion from IMCD cells measured by using a pH stat. These results provide direct evidence in freshly isolated IMCD cells that both a Na+:H+ antiporter and a rheogenic H(+)-ATPase participate in pHi regulation.

Pressure-induced smooth muscle cell depolarization in pulmonary arteries from control and chronically hypoxic rats does not cause myogenic vasoconstriction

2005 ◽  
Vol 98 (3) ◽  
pp. 1119-1124 ◽  
Author(s):  
Jay S. Naik ◽  
Scott Earley ◽  
Thomas C. Resta ◽  
Benjimen R. Walker
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Cell Membrane ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Pulmonary Arteries ◽  
Barometric Pressure ◽  
Cell Membrane Potential ◽  
Intraluminal Pressure ◽  
Dose Dependent

Chronic obstructive pulmonary diseases, as well as prolonged residence at high altitude, can result in generalized airway hypoxia, eliciting an increase in pulmonary vascular resistance. We hypothesized that a portion of the elevated pulmonary vascular resistance following chronic hypoxia (CH) is due to the development of myogenic tone. Isolated, pressurized small pulmonary arteries from control (barometric pressure ≅ 630 Torr) and CH (4 wk, barometric pressure = 380 Torr) rats were loaded with fura 2-AM and perfused with warm (37°C), aerated (21% O2-6% CO2-balance N2) physiological saline solution. Vascular smooth muscle (VSM) intracellular Ca2+ concentration ([Ca2+]i) and diameter responses to increasing intraluminal pressure were determined. Diameter and VSM cell [Ca2+]i responses to KCl were also determined. In a separate set of experiments, VSM cell membrane potential responses to increasing luminal pressure were determined in arteries from control and CH rats. VSM cell membrane potential in arteries from CH animals was depolarized relative to control at each pressure step. VSM cells from both groups exhibited a further depolarization in response to step increases in intraluminal pressure. However, arteries from both control and CH rats distended passively to increasing intraluminal pressure, and VSM cell [Ca2+]i was not affected. KCl elicited a dose-dependent vasoconstriction that was nearly identical between control and CH groups. Whereas KCl administration resulted in a dose-dependent increase in VSM cell [Ca2+]i in arteries taken from control animals, this stimulus elicited only a slight increase in VSM cell [Ca2+]i in arteries from CH animals. We conclude that the pulmonary circulation of the rat does not demonstrate pressure-induced vasoconstriction.

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