Influence of microgeometry on membrane potential of shaly sands

Geophysics ◽  
1989 ◽  
Vol 54 (12) ◽  
pp. 1543-1553 ◽  
Author(s):  
Pabitra N. Sen
Keyword(s):  
Membrane Potential ◽  
Pore Space ◽  
Geometrical Parameters ◽  
Formation Factor ◽  
Empirical Formulas ◽  
Water Conductivity ◽  
Shaly Sand ◽  
Local Geology ◽  
Geometrical Factors

The microgeometry of the pore space influences the membrane potential [Formula: see text] and the dc electrical conductivity σ of a shaly sand in a similar manner, independent of the details of the geometry. [Formula: see text] and σ are related via the conductivities of cations and anions [Formula: see text] and [Formula: see text], and [Formula: see text]. This explicit relationship is used to investigate the role of the geometrical factors that influence both [Formula: see text] and σ in a related manner. The dependence of σ on water conductivity [Formula: see text] can be well approximated with four geometrical parameters, which can be obtained from the slopes and the intercepts of curves of σ versus [Formula: see text] at high and low salinities. I show how these geometrical factors appear in the expression for [Formula: see text] as well. The geometrical parameters, one of them being the formation factor, vary from rock to rock; and any trend in the parameters depends on the local geology. For the data on a group of 140 different cores, the geometrical factors could be well approximated by functions of porosity, cementation exponent, and charge density, to give a simple conductivity formula analogous to the empirical formulas that are most widely used in formation evaluation. These empirical factors are used to obtain an approximate formula for [Formula: see text].

Influence of Microgeometry on Membrane Potential of Shaly Sands

1990 ◽  
Vol 195 ◽  
Author(s):  
Pabitra N. Sen
Keyword(s):  
Electrical Conductivity ◽  
Membrane Potential ◽  
Pore Space ◽  
Geometrical Parameters ◽  
Formation Factor ◽  
Water Conductivity ◽  
Shaly Sand ◽  
Local Geology ◽  
Geometrical Factors

ABSTRACTThe microgeometry of the pore space influences the membrane potential Em. and theDC electrical conductivity σ of a shaly sand in a similar manner, independent of the details of the geometry: Em and σ being related via the conductivities of cations and σanions;σ=σcation + σ onion, and Em α σ cation/(σcation + σanion). This explicit relationship is used to investigate the role of the geometrical factors which influence both Em and σ in a related manner. The dependence of σ on the water conductivity σw can be well approximated with four geometrical parameters which can be obtained from the slopes and the interceptsof σ vs. σw curve at high and low salinities. We show that these geometrical factors appear in the expression for Em a well. These geometrical parameters (one of them is the formation factor) vary from rock to rock, and any trend in these parameters depend on the local geology.

Correspondence between membrane potential and conductivity

Geophysics ◽  
1991 ◽  
Vol 56 (4) ◽  
pp. 461-471 ◽  
Author(s):  
P. N. Sen
Keyword(s):  
Membrane Potential ◽  
Transport Number ◽  
Activity Ratio ◽  
Ionic Concentration ◽  
Salinity Range ◽  
Liquid Junction Potential ◽  
Formation Factor ◽  
Liquid Junction ◽  
Water Conductivity ◽  
Junction Potential

Combining the membrane potential [Formula: see text] with the corresponding ideal membrane potential [Formula: see text] and the liquid junction potential [Formula: see text], for the same activity ratio, gives [Formula: see text]. [Formula: see text] and [Formula: see text] are the reciprocal of the average of the reciprocal water conductivity and reciprocal of cation and anion conductivities, and [Formula: see text]; and [Formula: see text] is the average of the ratio of the water to the rock conductivity [Formula: see text] with respect to [Formula: see text], where t is the transport number for the Na ion, [Formula: see text] is the ionic concentration, and [Formula: see text] is the activity coefficient. This relationship is independent of any model and does not even refer to the value of clay counterion concentration. Combining σ with [Formula: see text] gives the saturation dependent formation factor F, and thus the interpretation of shaly sands becomes no more difficult than for clean sands. Experimental data on 27 rocks for which both membrane potential and conductivity were measured by Smits (1968) and Waxman and Smits (1968) over a large salinity range are used to verify this relationship.

scholarly journals Intracellular Na+ Modulates Pacemaking Activity in Murine Sinoatrial Node Myocytes: An In Silico Analysis

2021 ◽  
Vol 22 (11) ◽  
pp. 5645
Author(s):  
Stefano Morotti ◽  
Haibo Ni ◽  
Colin H. Peters ◽  
Christian Rickert ◽  
Ameneh Asgari-Targhi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Membrane Potential ◽  
In Silico ◽  
Sinoatrial Node ◽  
In Silico Analysis ◽  
Ankyrin B ◽  
Deficient Mice ◽  
Silico Analysis ◽  
Bursting Activity

Background: The mechanisms underlying dysfunction in the sinoatrial node (SAN), the heart’s primary pacemaker, are incompletely understood. Electrical and Ca2+-handling remodeling have been implicated in SAN dysfunction associated with heart failure, aging, and diabetes. Cardiomyocyte [Na+]i is also elevated in these diseases, where it contributes to arrhythmogenesis. Here, we sought to investigate the largely unexplored role of Na+ homeostasis in SAN pacemaking and test whether [Na+]i dysregulation may contribute to SAN dysfunction. Methods: We developed a dataset-specific computational model of the murine SAN myocyte and simulated alterations in the major processes of Na+ entry (Na+/Ca2+ exchanger, NCX) and removal (Na+/K+ ATPase, NKA). Results: We found that changes in intracellular Na+ homeostatic processes dynamically regulate SAN electrophysiology. Mild reductions in NKA and NCX function increase myocyte firing rate, whereas a stronger reduction causes bursting activity and loss of automaticity. These pathologic phenotypes mimic those observed experimentally in NCX- and ankyrin-B-deficient mice due to altered feedback between the Ca2+ and membrane potential clocks underlying SAN firing. Conclusions: Our study generates new testable predictions and insight linking Na+ homeostasis to Ca2+ handling and membrane potential dynamics in SAN myocytes that may advance our understanding of SAN (dys)function.

Effect of low chloride on relaxation in hamster diaphragm muscle

1986 ◽  
Vol 61 (1) ◽  
pp. 180-184 ◽  
Author(s):  
S. A. Esau ◽  
N. Sperelakis
Keyword(s):  
Membrane Potential ◽  
Muscle Fatigue ◽  
Time Constant ◽  
Diaphragm Muscle ◽  
Resting Membrane Potential ◽  
Krebs Solution ◽  
Sarcolemmal Membrane ◽  
Cl Conductance

With muscle fatigue the chloride (Cl-) conductance of the sarcolemmal membrane decreases. The role of lowered Cl- conductance in the prolongation of relaxation seen with fatigue was studied in isolated hamster diaphragm strips. The muscles were studied in either a Krebs solution or a low Cl- solution in which half of the NaCl was replaced by Na-gluconate. Short tetanic contractions were produced by a 160-ms train of 0.2-ms pulses at 60 Hz from which tension (T) and the time constant of relaxation were measured. Resting membrane potential (Em) was measured using KCl-filled microelectrodes with resistances of 15–20 M omega. Mild fatigue (20% fall in tension) was induced by 24–25 tetanic contractions at the rate of 2/s. There was no difference in Em or T in the two solutions, either initially or with fatigue. The time constant of relaxation was greater in low Cl- solution, both initially (22 +/- 3 vs. 18 +/- 5 ms, mean +/- SD, P less than 0.05) and with fatigue (51 +/- 18 vs. 26 +/- 7 ms, P less than 0.005). Lowering of sarcolemmal membrane Cl- conductance appears to play a role in the slowing of relaxation of hamster diaphragm muscle seen with fatigue.

Regulation of intracellular calcium in N1E-115 neuroblastoma cells: the role of Na+/Ca2+exchange

2002 ◽  
Vol 282 (5) ◽  
pp. C1000-C1008 ◽  
Author(s):  
Kara L. Kopper ◽  
Joseph S. Adorante
Keyword(s):  
Membrane Potential ◽  
Intracellular Calcium ◽  
Normal Cell ◽  
Buffer Capacity ◽  
Neuroblastoma Cells ◽  
Fold Increase ◽  
Scorpion Venom ◽  
Reverse Mode ◽  
Intracellular Ca

In fura 2-loaded N1E-115 cells, regulation of intracellular Ca2+ concentration ([Ca2+]i) following a Ca2+ load induced by 1 μM thapsigargin and 10 μM carbonylcyanide p-trifluoromethyoxyphenylhydrazone (FCCP) was Na+ dependent and inhibited by 5 mM Ni2+. In cells with normal intracellular Na+ concentration ([Na+]i), removal of bath Na+, which should result in reversal of Na+/Ca2+exchange, did not increase [Ca2+]i unless cell Ca2+ buffer capacity was reduced. When N1E-115 cells were Na+ loaded using 100 μM veratridine and 4 μg/ml scorpion venom, the rate of the reverse mode of the Na+/Ca2+ exchanger was apparently enhanced, since an ∼4- to 6-fold increase in [Ca2+]ioccurred despite normal cell Ca2+ buffering. In SBFI-loaded cells, we were able to demonstrate forward operation of the Na+/Ca2+ exchanger (net efflux of Ca2+) by observing increases (∼ 6 mM) in [Na+]i. These Ni2+ (5 mM)-inhibited increases in [Na+]i could only be observed when a continuous ionomycin-induced influx of Ca2+ occurred. The voltage-sensitive dye bis-(1,3-diethylthiobarbituric acid) trimethine oxonol was used to measure changes in membrane potential. Ionomycin (1 μM) depolarized N1E-115 cells (∼25 mV). This depolarization was Na+dependent and blocked by 5 mM Ni2+ and 250–500 μM benzamil. These data provide evidence for the presence of an electrogenic Na+/Ca2+ exchanger that is capable of regulating [Ca2+]i after release of Ca2+ from cell stores.

scholarly journals Role of Ca+-dependent K-channels in the membrane potential and contractility of aorta from spontaneously hypertensive rats

1994 ◽  
Vol 113 (3) ◽  
pp. 1022-1028 ◽  
Author(s):  
Eneida G. Silva ◽  
Eugenio Frediani-Neto ◽  
Alice T. Ferreira ◽  
Antonio CM. Paiva ◽  
Therezinha B. Paiva
Keyword(s):  
Membrane Potential ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
K Channels

Modulation of neuronal mitochondrial membrane potential by the NMDA receptor: role of arachidonic acid

1997 ◽  
Vol 777 (1-2) ◽  
pp. 69-74 ◽  
Author(s):  
Antonio Camins ◽  
Francesc X Sureda ◽  
Cecilia Gabriel ◽  
Mercè Pallàs ◽  
Elena Escubedo ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Membrane Potential ◽  
Nmda Receptor ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane

scholarly journals Cytoplasmic [Ca2+] and intracellular pH in lymphocytes. Role of membrane potential and volume-activated Na+/H+ exchange.

1987 ◽  
Vol 89 (2) ◽  
pp. 185-213 ◽  
Author(s):  
S Grinstein ◽  
S Cohen
Keyword(s):  
Protein Kinase C ◽  
Membrane Potential ◽  
Protein Kinase ◽  
Intracellular Ph ◽  
Enzyme Treatment ◽  
Membrane Hyperpolarization ◽  
Kinase C ◽  
Free Media ◽  
Stimulation Of

The effect of elevating cytoplasmic Ca2+ [( Ca2+]i) on the intracellular pH (pHi) of thymic lymphocytes was investigated. In Na+-containing media, treatment of the cells with ionomycin, a divalent cation ionophore, induced a moderate cytoplasmic alkalinization. In the presence of amiloride or in Na+-free media, an acidification was observed. This acidification is at least partly due to H+ (equivalent) uptake in response to membrane hyperpolarization since: it was enhanced by pretreatment with conductive protonophores, it could be mimicked by valinomycin, and it was decreased by depolarization with K+ or gramicidin. In addition, activation of metabolic H+ production also contributes to the acidification. The alkalinization is due to Na+/H+ exchange inasmuch as it is Na+ dependent, amiloride sensitive, and accompanied by H+ efflux and net Na+ gain. A shift in the pHi dependence underlies the activation of the antiport. The effect of [Ca2+]i on Na+/H+ exchange was not associated with redistribution of protein kinase C and was also observed in cells previously depleted of this enzyme. Treatment with ionomycin induced significant cell shrinking. Prevention of shrinking largely eliminated the activation of the antiport. Moreover, a comparable shrinking produced by hypertonic media also activated the antiport. It is concluded that stimulation of Na+/H+ exchange by elevation of [Ca2+]i is due, at least in part, to cell shrinking and does not require stimulation of protein kinase C.

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