Modeling of the Short Circuit Impedance on the Base of TRV time course

Author(s):  
Zbigniew Pochanke ◽  
Szymon Stoczko ◽  
Tadeusz Daszczynski
1979 ◽  
Vol 78 (1) ◽  
pp. 1-27
Author(s):  
MAURIZIO MIROLLI

1. The input properties and the response to stretch of a coxal receptor, the S fibre of the crab Scylla serrata, were studied using two and three intracellular microelectrodes. 2. In the relaxed receptor the transmembrane potential ranged from about −60 to −70 mV, and the input resistance, RT, from 1 to 3 MΩ. The input IV relationship, studied by injecting slow-rising current ramps, was not linear either in the hyperpolarizing or in the depolarizing quadrants. 3. Low values of RT and a linear IV relationship were associated with a large leakage of the microelectrodes. 4. The response to step stretches was complex, consisting of an initial depolarizing transient, Vα, and a steady-state depolarizing plateau, V8. Both Vα and V8 propagated with decrement in the fibre which was about 9 mm long. The spatial decrement of Vα and V8 was equal to that of the response to distally injected current pulses of comparable duration and amplitude. 5. On the basis of the spatial decrement of both Vα and V8 the dendrite can be considered equivalent, for current flowing from its distal to its proximal end, to a semi-infinite cable having a length constant of between 4 and 6 cm. 6. The voltage transients recorded in response to long current pulses reached 84% of their final value in a time (t84%) ranging from 150 to 180 ms in fibres in which RT was 2 Mω or larger. t84% was smaller in fibres having a lower RT. 7. The time course of the transients recorded in response to injected current pulses deviated from the semi-infinite cable model in a manner suggesting the presence of a partial short circuit. For this reason the membrane time constant of the fibre is considered larger (by an undetermined amount) than t84%. 8. The fibre presented less resistance to current flowing from its proximal to its distal end than to current flowing in the opposite direction. For this reason, and also because of the time course of the voltage transient, it is concluded that the distal sensory endings of the fibre have the properties of a leaky end termination, even in the non-stimulated receptors.


2003 ◽  
Vol 150 (2) ◽  
pp. 169 ◽  
Author(s):  
K.O.H. Pedersen ◽  
A.H. Nielsen ◽  
N.K. Poulsen

1997 ◽  
Vol 272 (4) ◽  
pp. C1169-C1177 ◽  
Author(s):  
W. Jin ◽  
U. Hopfer

The involvement of cytosolic Ca2+ concentration ([Ca2+]i) as messenger for the regulation of Na+-K+-ATPase activity was investigated in a renal cell line recently developed by immortalization of early proximal tubule primary cultures from the Wistar-Kyoto rat strain. Na+-K+-ATPase was measured as short-circuit current (Isc) in intact monolayers after permeabilization of the apical plasma membrane with amphotericin B. With symmetrical solutions, Isc quantitatively reflects Na+-K+-ATPase activity as judged by ouabain inhibition and dependence on Na+ and K+. Extracellular ATP (50% effective concentration = 0.32 mM) on the apical side produced acute inhibition of Na+-K+-ATPase-generated Isc of up to 50%. The inhibition peaked within 1 min and lasted approximately 5 min. The potency order was ATP > ADP >> beta,gamma-methyleneadenosine 5'-triphosphate = UTP, consistent with a P2y receptor. Extracellular ATP also stimulated a transient increase in [Ca2+]i. This increase had a similar time course as the inhibition of ATPase and reached a peak change of approximately 120 nM. However, the elevation of [Ca2+]i is not required in the purinergic inhibition of the Na+-K+-ATPase, since, first, increases in [Ca2+]i produced with a Ca2+ ionophore (ionomycin) failed to mimic the purinergic inhibition and, second, 1,2-bis(2-aminophenoxy)-ethane-N,N,N',N'-tetraacetic acid, which abolished the [Ca2+]i elevation, failed to block the purinergic inhibition.


Author(s):  
Yang Liu ◽  
Zijian Yin ◽  
Qiang Gao ◽  
Xingjun Tian ◽  
Xiaoxuan Yang

1992 ◽  
Vol 263 (4) ◽  
pp. R827-R833 ◽  
Author(s):  
T. C. Cox

The larval frog skin has a very high electrical resistance and a corresponding low rate of transepithelial ion transport. Amiloride, a blocker of sodium transport in adult skin, transiently stimulates rather than inhibits short-circuit current (Isc) across larval skin. The time course and concentration response to amiloride and the effects of calcium channel blockers on Isc were studied with larval frog skin mounted in modified Ussing chambers. The amiloride (1 mM) transient was markedly blunted if the skin was previously exposed to low amiloride (0.01-0.1 mM) concentrations. The calcium channel blockers verapamil, nitrendipine, diltiazem, W-7, and lanthanum all blocked the amiloride transient. Diltiazem itself caused a rapid transient in Isc, indicating that it may be a partial agonist. These data suggest that the amiloride-stimulated cation channels rapidly desensitize in a manner similar to the acetylcholine receptor. The decline in Isc after amiloride stimulation could be caused by amiloride block of the open channel. Blockade of amiloride stimulation by well-known calcium channel blockers suggests that these larval cation channels may have some characteristics in common with calcium channels.


1981 ◽  
Vol 240 (3) ◽  
pp. C103-C105 ◽  
Author(s):  
J. S. Handler ◽  
F. M. Perkins ◽  
J. P. Johnson

Three continuous lines of amphibian epithelial cells form epithelia with a high transepithelial resistance (greater than 4,000 omega . cm2) in culture. The cell lines are TB-M and TB-6c, derived from the urinary bladder of Bufo marinus, and A6, derived from the kidney of Xenopus laevis. Short-circuit current is equivalent to net mucosa-to-serosa sodium transport in two cell lines and slightly exceeds sodium transport in epithelia formed by TB-6c cells. None of the cell lines has an adenylate cyclase response or a transport or permeability response to vasopressin. Water permeability is low in all three cell lines and is not affected by adenosine 3',5–-cyclic monophosphate (cAMP). In the three lines of cells, cAMP and aldosterone each increases short-circuit current with a time course similar to that seen in naturally occurring epithelia. In contrast to the toad urinary bladder and epithelia of line TB-M in which the aldosterone stimulation of short-circuit current is associated with a fall in transepithelial resistance, there is no change in resistance across epithelia of lines TB-6c and A6. There is also a striking difference in the sensitivity of the three lines to inhibition of short-circuit current by amiloride.


1987 ◽  
Vol 252 (5) ◽  
pp. C468-C476 ◽  
Author(s):  
M. P. Paccolat ◽  
K. Geering ◽  
H. P. Gaeggeler ◽  
B. C. Rossier

The effects of aldosterone on transepithelial sodium transport (measured by the short-circuit current (SCC) and on Na+-K+-adenosine triphosphatase (ATPase) biogenesis have been studied in A6 kidney cells grown on collagen-coated filters in two different media. In medium A, base-line SCCA was close to zero but transmural electrical resistance (RA) was high. Aldosterone (100 nM, t24h) drastically increased SCCA and RA, but only after a 4-h latent period. In medium B, base-line SCCB and RB were significantly higher than in medium A. Aldosterone significantly enhanced SCCB and to a lesser extent RB after a much shorter latent period (approximately 45 min) than in medium A. In medium A, aldosterone elicited a fourfold increase in the relative rate of synthesis of alpha- and beta-subunits of Na+-K+-ATPase. A twofold increase was already observed within the observed latent period. This time course suggests that de novo synthesis of sodium pumps might be one of the critical factors underlying the increase in sodium transport in this growth medium. In medium B, aldosterone elicited a two- to fourfold increase in the relative rate of synthesis of the alpha- and beta-subunits of Na+-K+-ATPase that paralleled SCCB. Thus de novo synthesis of Na+-K+-ATPase is clearly not a prerequisite for the early mineralocorticoid response (t90 min - t180 min), but still could be part of the late mineralocorticoid response (t3 h - t24 h). In both media, the immunochemical cellular pool of Na+-K+-ATPase was apparently not modulated by aldosterone for up to 48 h of incubation.(ABSTRACT TRUNCATED AT 250 WORDS)


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