Electrophysiology of mammalian gland cells

1976 ◽  
Vol 56 (3) ◽  
pp. 535-577 ◽  
Author(s):  
O. H. Petersen
Keyword(s):  
Membrane Potential ◽  
Cell Membrane ◽  
Concentration Gradient ◽  
Gland Cell ◽  
Membrane Resistance ◽  
Transport Processes ◽  
Receptor Interaction ◽  
Cellular Transport ◽  
Gland Cells ◽  
Surface Cell

The resting cell membrane potential varies from -40 to -70 mV according to type of gland cell and species. The RP depends mainly on the large transmembrane concentration gradient for K maintained by a pump mechanism extruding Na and accumulating K. Since the Na permeability (PNa) is much smaller than PK, the Na concentration gradient is less important. In addition to the dominant electrodiffusional control of RP the Na pump itself contributes since the active transport of Na (out) exceeds that of the active K uptake. Gland cells are generally electrically coupled--i.e., the junctional membrane resistance is much lower than the surface membrane resistance. The coupling may be widespread (e.g., liver) or confined to one acinus (e.g., salivary gland and pancreas). The specific surface cell membrane resistance may be about 2000 omega cm2. A number of neurotransmitters and hormones control cellular transport processes by their action on surface cell membrane receptors. Agonist-receptor interaction causes prominent changes in membrane potential and resistance, in many cases of a complex nature. Most gland cell membranes so far investigated in detail appear to be electrically inexcitable; i.e., stimulation does not cause the appearance of action potentials (e.g., salivary glands, exocrine pancreas, and liver) but prominent exceptions to this are the endocrine pancreas (beta-cells) and the adrenal cortex. The main importance of agonist-induced membrane permeability changes is to alter the intracellular ion activities. An increase in [Na+] seems to be important whenever stimulation results in fluid transport and an increase in [Ca2+] triggers exocytosis.

scholarly journals The mechanism of the NH4 ion oscillatory transport across the excitable cell membrane

2005 ◽  
pp. 5-19
Author(s):  
Cedomir Radenovic ◽  
Milos Beljanski ◽  
Georgij Maksimov ◽  
Aleksandar Kalauzi ◽  
Milan Drazic
Keyword(s):  
Membrane Potential ◽  
Cell Membrane ◽  
Transport Processes ◽  
Excitable Cell ◽  
Direct Dependence ◽  
Nh4cl Solution ◽  
Oscillatory Processes

This paper presents results on typical oscillations of the membrane potential induced by the excitation of the cell membrane by different concentrations of the NH4Cl solution. The existence of four classes of oscillations of the membrane potential and several different single and local impulses rhythmically occurring were determined. It is known that the oscillatory processes of the membrane potential are in direct dependence on oscillatory transport processes of NH4 and Cl ions across the excitable cell membrane. A hypothesis on a possible mechanism of oscillatory transport processes of NH4 and Cl ions across the excitable cell membrane is also presented.

Measurement of intracellular Ca2+ activity in Necturus gallbladder

1987 ◽  
Vol 253 (2) ◽  
pp. C309-C315 ◽  
Author(s):  
C. E. Palant ◽  
I. Kurtz
Keyword(s):  
Membrane Potential ◽  
Cell Membrane ◽  
Membrane Resistance ◽  
Cell Membrane Potential ◽  
Transepithelial Resistance ◽  
Cell Membrane Permeability ◽  
Significant Drop ◽  
Electrophysiological Properties ◽  
Leaky Epithelia ◽  
Necturus Gallbladder

To clarify the effects of Ca2+-free solutions on the electrophysiological properties of leaky epithelia, Necturus gallbladder was mounted in an Ussing-type chamber and its mucosal surface exposed to Ca2+-free EGTA (2 mM) Ringer. Lateral-space width was controlled by a -3-cmH2O pressure gradient on the serosal outflow. Transepithelial potential difference and resistance were monitored while cell membrane potential and intracellular Ca2+ activity (Ca2+i) were determined with conventional and Ca2+-sensitive microelectrodes. Ca2+i averaged 183 +/- 27 nM (n = 15). Reduction of mucosal Ca2+ activity to approximately 500 nM reversibly lowered transepithelial resistance while cell membrane potential remained unaltered and fractional membrane resistance increased from 0.77 +/- 0.01 to 0.83 +/- 0.02 (P less than 0.01, n = 5). In five gallbladders mucosal Ca2+ reduction induced a significant drop in Ca2+i from 133 +/- 26 to 77 +/- 20 nM (P less than 0.01, n = 5) while transepithelial resistance fell from 125 +/- 27 to 107 +/- 24 omega X cm2 (P less than 0.01). These results indicate that transepithelial resistance decrements observed during exposure to Ca2+-free solutions stem from a reversible increase in tight-junctional but not cell membrane permeability and that this effect is associated with a fall in intracellular Ca2+ activity.

Unusual potassium channels mediate nonadrenergic noncholinergic nerve-mediated inhibition in opossum esophagus

1985 ◽  
Vol 63 (2) ◽  
pp. 107-112 ◽  
Author(s):  
J. Jury ◽  
L. P. Jager ◽  
E. E. Daniel
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Cell Membrane ◽  
Guinea Pig ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Membrane Resistance ◽  
Potassium Ion ◽  
Ion Permeability ◽  
Muscle Cell Membrane

Field stimulation of the circular muscle of the opossum esophagus produces a transient hyperpolarization (inhibitory junction potential, IJP) followed by an "off" depolarization. A similar nonadrenergic, noncholinergic (NANC) response in guinea pig taenia caecum has been shown to be due to an increase in the potassium ion permeability of the smooth muscle cell membrane. Double sucrose gap studies showed a decrease in resistance during the IJP, and a reversal at an estimated membrane potential of about −90 mV (4 mM K+). The reversal potential was dependent on the extracellular potassium concentration, shifting to −75 mV when the potassium in the superfusion medium was increased to 10 mM. The IJP in the opossum esophageal circular smooth muscle is therefore like the IJP of the guinea pig taenia caecum in that it is probably due to a selective increase in potassium ion permeability. Potassium conductance blocking agents, tetraethylammonium chloride (TEA, 20 mM) and 4-aminopyridine (4-AP, 5 mM) both caused a depolarization of the smooth muscle cell membrane, but TEA increased the membrane resistance, whereas 4-AP did not affect the membrane conductance in a consistent way. A decrease in IJP amplitude owing to these agents was not apparent. Apamin (10 μM) did not affect the membrane potential, the membrane resistance, or the IJP. Quinine (0.1 mM) produced effects quantitatively similar to those of TEA. Quinine (1 mM) did abolish the IJP, however, this was likely due to a blockade of impulse transmission of the intramural nerves. These results suggest that the receptor-operated channels opened by the NANC-nerve mediator in this tissue are unusual in that they are different from those functioning to maintain the resting membrane potential and they differ from those involved in the IJP in the guinea pig taenia caecum.

scholarly journals Variable mechanisms of action of lithium during generating of membrane potential oscilations across the excitable membrane of the Nitela cell

2012 ◽  
pp. 101-114
Author(s):  
Cedomir Radenovic ◽  
Milos Beljanski ◽  
Georgij Maksimov ◽  
Dragomir Stanisavljev
Keyword(s):  
Membrane Potential ◽  
Cell Membrane ◽  
Mechanisms Of Action ◽  
Transport Processes ◽  
Excitable Membrane ◽  
Potential Oscillations ◽  
Excitable Cell ◽  
Lithium Transport ◽  
Membrane Potential Oscillations

This study presents results on variable mechanisms of lithium transport processes during generating of membrane potential oscillations across the very excitable membrane of the Nittela cell. Generating of several classes of oscillations, single and local impulses of the membrane potential, were presented in dependence on effects of a high LiCl concentration (10 mM), with which the cell membrane is very excited. Results on membrane potential oscillations are presented, and then some of oscillogram parameters were displayed. The assertion is that oscillations of the membrane potential are caused by total oscillatory transport processes: Li+, K+, Na+ and Cl-across the very excitable cell membrane. The paper presents the hypothesis on mechanisms of oscillatory transport processes of ions (Li, Na, K and Cl) expressed over different classes of oscillations, single and local impulses of the membrane potential across the excitable membrane of the Nittela cell.

scholarly journals Imaging the transmembrane and transendothelial sodium gradients in gliomas

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Muhammad H. Khan ◽  
John J. Walsh ◽  
Jelena M. Mihailović ◽  
Sandeep K. Mishra ◽  
Daniel Coman ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Magnetic Resonance ◽  
Cell Membrane ◽  
Normal Tissue ◽  
Magnetic Resonance Spectroscopic Imaging ◽  
Biological Factors ◽  
High Sodium ◽  
Intracellular Milieu

AbstractUnder normal conditions, high sodium (Na+) in extracellular (Na+e) and blood (Na+b) compartments and low Na+ in intracellular milieu (Na+i) produce strong transmembrane (ΔNa+mem) and weak transendothelial (ΔNa+end) gradients respectively, and these manifest the cell membrane potential (Vm) as well as blood–brain barrier (BBB) integrity. We developed a sodium (23Na) magnetic resonance spectroscopic imaging (MRSI) method using an intravenously-administered paramagnetic polyanionic agent to measure ΔNa+mem and ΔNa+end. In vitro 23Na-MRSI established that the 23Na signal is intensely shifted by the agent compared to other biological factors (e.g., pH and temperature). In vivo 23Na-MRSI showed Na+i remained unshifted and Na+b was more shifted than Na+e, and these together revealed weakened ΔNa+mem and enhanced ΔNa+end in rat gliomas (vs. normal tissue). Compared to normal tissue, RG2 and U87 tumors maintained weakened ΔNa+mem (i.e., depolarized Vm) implying an aggressive state for proliferation, whereas RG2 tumors displayed elevated ∆Na+end suggesting altered BBB integrity. We anticipate that 23Na-MRSI will allow biomedical explorations of perturbed Na+ homeostasis in vivo.

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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