Tetraethylammonium Chloride

1990 ◽  
Vol 96 (2) ◽  
pp. 225-256 ◽  
Author(s):  
W K Chandler ◽  
C S Hui

In experiments on cut muscle fibers mounted in a double Vaseline-gap chamber, electrical measurements are usually made by measuring the voltage V1(t) in one end pool and by passing current I2(t) from the other end pool to the central pool, which is usually clamped to earth potential. The voltage in the current-passing end pool is denoted by V2(t). This article describes how the value of the holding current, Ih, and the values of delta V2(infinity)/delta V1(infinity) and delta I2(infinity)/delta V1(infinity) that are associated with a small change in V1(t) can be used to estimate the linear cable parameters rm, ri, and re in a cut fiber that has been equilibrated with a Cs-containing internal solution. rm, ri, and re represent, respectively, the resistance of the plasma membranes, the internal longitudinal resistance, and the external longitudinal resistance under the Vaseline seals, all for a unit length of fiber. The apparent capacitance, Capp, of the preparation is defined to equal integral of infinity 0 delta I2,tr(t) dt/delta V1(infinity), in which delta I2,tr(t) represents the transient component of current that is associated with a change in V1(t) of amplitude delta V1(infinity). A method is described to estimate cm, the capacitance of the plasma membranes per unit length of fiber, from Capp and the values of rm, ri, and re. In experiments carried out with a tetraethylammonium chloride (TEA.Cl) solution at 13-14 degrees C in the central pool, cm remained stable for as long as 3-4 h. The values of cm, 0.19 microF/cm on average, and their variation with fiber diameter are similar to published results from intact fibers. This article also describes the different pathways that are taken by the current that flows from the current-passing end pool to the central pool. Approximately two-thirds of delta I2,tr(t) flows across the capacitance of the plasma membranes in the central-pool region. The rest flows either across plasma membranes that are under the two Vaseline seals or directly from the current-passing end pool to the central pool, across the external longitudinal resistance under the Vaseline seal. [There is also a current that flows directly from the voltage-measuring end pool to the central pool but this does not contribute to delta I2,tr(t).]


2003 ◽  
Vol 284 (4) ◽  
pp. H1080-H1086 ◽  
Author(s):  
John J. Bosnjak ◽  
Ken Terata ◽  
Hiroto Miura ◽  
Atsushi Sato ◽  
Alfred C. Nicolosi ◽  
...  

Thrombin (Thromb), activated as part of the clotting cascade, dilates conduit arteries through an endothelial pertussis toxin (PTX)-sensitive G-protein receptor and releases nitric oxide (NO). Thromb also acts on downstream microvessels. Therefore, we examined whether Thromb dilates human coronary arterioles (HCA). HCA from right atrial appendages were constricted by 30–50% with endothelin-1. Dilation to Thromb (10−4–1 U/ml) was assessed before and after inhibitors with videomicroscopy. There was no tachyphylaxis to Thromb dilation (maximum dilation = 87.0%, ED50 = 1.49 × 10−2). Dilation to Thromb was abolished with either hirudin or denudation but was not affected by PTX. Neither N ω-nitro-l-arginine methyl ester ( n = 7), indomethacin ( n = 9),1H-[1,2,4] oxadiazolo-[4,3-a]quinoxalin-1-one ( n = 6), tetraethylammonium chloride ( n = 5), nor iberiotoxin ( n = 4) reduced dilation to Thromb. However, KCl (maximum dilation = 89 ± 5 vs. 20 ± 10%; P < 0.05; n = 7), tetrabutylammonium chloride (maximum dilation = 79 ± 7 vs. 21 ± 4%; P < 0.05; n = 5), and charybdotoxin (maximum dilation = 89 ± 4 vs. 10 ± 2%; P < 0.05; n = 4) attenuated dilation to Thromb. In contrast to animal models, Thromb-induced dilation in human arterioles is independent of Gi-protein activation and NO release. However, Thromb dilation is endothelium dependent, is maintained on consecutive applications, and involves activation of K+ channels. We speculate that an endothelium-derived hyperpolarizing factor contributes to Thromb-induced dilation in HCA.


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