Modulation of cell membrane potential in cultured vascular endothelium

1996 ◽  
Vol 270 (3) ◽  
pp. C819-C824 ◽  
Author(s):  
L. Vaca ◽  
A. Licea ◽  
L. D. Possani
Keyword(s):  
Membrane Potential ◽  
Cell Membrane ◽  
Cell Membrane Potential ◽  
Resting Potential ◽  
Similar Response ◽  
Aortic Endothelial Cells ◽  
Ionic Conductances ◽  
Selective Channel ◽  
Inwardly Rectifying

The present study explores the role of different ionic conductances in the regulation of membrane potential under resting conditions and after bradykinin (BK) or thapsigargin (TG) stimulation of cultured bovine aortic endothelial cells. Under resting conditions, the cell membrane potential observed was -62+/- 5 mV. The main conductance under these conditions is an inwardly rectifying potassium (IRK) channel. Application of 50 nM BK induced a transient hyperpolarization to -87 +/- 4 mV followed by sustained depolarization to -35 +/- 5 mV. The transient hyperpolarization was eliminated by 1 microM noxiustoxin, a blocker of calcium-activated postassium channels (K(Ca)). the sustained depolarization induced by BK was prevented by incubating the cells with the calcium channel blocker lanthanum. TG evoked a similar response in membrane potential, with the exception that the onset of the hyperpolarization was slower compared with BK. The results presented here indicate that the cell resting potential is maintained at -62 +/- 2 mV by the IRK channel. BK or TG stimulation induces a transient hyperpolarization of approximately -20 mV produced by activation of a KCa. This hyperpolarization is followed by a sustained depolarization produced by activation of a calcium-selective channel sensitive to lanthanum.

A small synthetic molecule forms selective potassium channels to regulate cell membrane potential and blood vessel tone

2014 ◽  
Vol 12 (41) ◽  
pp. 8174-8179 ◽  
Author(s):  
Hui-Yan Zha ◽  
Bing Shen ◽  
Kwok-Hei Yau ◽  
Shing-To Li ◽  
Xiao-Qiang Yao ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Potassium Channels ◽  
Cell Membrane ◽  
Blood Vessel ◽  
Muscle Cell ◽  
Cell Membrane Potential ◽  
Vascular Muscle ◽  
Selective Channel ◽  
Synthetic Molecule ◽  
Muscle Cell Membrane

A molecule forms a K+-selective channel in the cell membrane to regulate vascular muscle cell membrane potential and blood vessel tone.

scholarly journals β CELL MEMBRANE POTENTIAL AND INSULIN RELEASE; ROLE OF CALCIUM AND CALCIUM: MAGNESIUM RATIO

1983 ◽  
Vol 68 (2) ◽  
pp. 233-245 ◽  
Author(s):  
Illani Atwater ◽  
Barbara J. Frankel ◽  
Eduardo Rojas ◽  
Gerold M. Grodsky
Keyword(s):  
Membrane Potential ◽  
Cell Membrane ◽  
Insulin Release ◽  
Cell Membrane Potential ◽  
Β Cell ◽  
Calcium Magnesium

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.

Pancreatic beta-cell electrical activity: the role of anions and the control of pH

1983 ◽  
Vol 244 (3) ◽  
pp. C188-C197 ◽  
Author(s):  
G. T. Eddlestone ◽  
P. M. Beigelman
Keyword(s):  
Membrane Potential ◽  
Cell Membrane ◽  
Beta Cell ◽  
Pancreatic Beta Cell ◽  
Proton Exchange ◽  
Disulfonic Acid ◽  
Control Mechanisms ◽  
Exchange System ◽  
Sodium Proton Exchange

The influence of chloride on the mouse pancreatic beta-cell membrane potential and the cell membrane mechanisms controlling intracellular pH (pHi) have been investigated using glass microelectrodes to monitor the membrane potential. It has been shown that chloride is distributed passively across the beta-cell membrane such that chloride potential is equal to the membrane potential. Withdrawal of perifusate chloride or bicarbonate and the application of the drugs 4-acetamido-4'-isethiocyanostilbene-2,2'-disulfonic acid (SITS) and probenecid, both blockers of transmembrane anion movement, have been used to establish that a chloride-bicarbonate exchange system is operative in the cell membrane and that it is one of the control mechanisms of pHi. Amiloride, a specific blocker of the transmembrane sodium proton exchange, has been used to demonstrate that this mechanism is also operative in the beta-cell membrane in the control of pHi. The hypothesis that the calcium-activated potassium permeability is proton sensitive at an intracellular site, a fall in pHi causing a fall in permeability and an increase in pHi causing an increase in permeability, has been used to explain many of the effects observed in this study.

Cell Membrane Potential Model Circuit Lab

2018 ◽  
Vol 56 (8) ◽  
pp. 540-543
Author(s):  
Mickey D. Kutzner ◽  
J. Michael Bryson
Keyword(s):  
Membrane Potential ◽  
Cell Membrane ◽  
Potential Model ◽  
Cell Membrane Potential ◽  
Model Circuit

scholarly journals Signaling mechanism by the Staphylococcus aureus two-component system LytSR: role of acetyl phosphate in bypassing the cell membrane electrical potential sensor LytS

F1000Research ◽  
2016 ◽  
Vol 4 ◽  
pp. 79 ◽  
Author(s):  
Kevin Patel ◽  
Dasantila Golemi-Kotra
Keyword(s):  
Staphylococcus Aureus ◽  
Membrane Potential ◽  
Cell Membrane ◽  
Electrical Potential ◽  
Cell Membrane Potential ◽  
Acetyl Phosphate ◽  
Two Component System ◽  
Component System ◽  
Two Component ◽  
Membrane Electrical Potential

The two-component system LytSR has been linked to the signal transduction of cell membrane electrical potential perturbation and is involved in the adaptation of Staphylococcus aureus to cationic antimicrobial peptides. It consists of a membrane-bound histidine kinase, LytS, which belongs to the family of multiple transmembrane-spanning domains receptors, and a response regulator, LytR, which belongs to the novel family of non-helix-turn-helix DNA-binding domain proteins. LytR regulates the expression of cidABC and lrgAB operons, the gene products of which are involved in programmed cell death and lysis. In vivo studies have demonstrated involvement of two overlapping regulatory networks in regulating the lrgAB operon, both depending on LytR. One regulatory network responds to glucose metabolism and the other responds to changes in the cell membrane potential. Herein, we show that LytS has autokinase activity and can catalyze a fast phosphotransfer reaction, with 50% of its phosphoryl group lost within 1 minute of incubation with LytR. LytS has also phosphatase activity. Notably, LytR undergoes phosphorylation by acetyl phosphate at a rate that is 2-fold faster than the phosphorylation by LytS. This observation is significant in lieu of the in vivo observations that regulation of the lrgAB operon is LytR-dependent in the presence of excess glucose in the medium. The latter condition does not lead to perturbation of the cell membrane potential but rather to the accumulation of acetate in the cell. Our study provides insights into the molecular basis for regulation of lrgAB in a LytR-dependent manner under conditions that do not involve sensing by LytS.

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