|
|
|
|
|
|
|
||
The Journal of General Physiology, Vol 83, 819-839, Copyright © 1984 by The Rockefeller University Press
ARTICLES |
AM Garcia and C Miller
The permeability of isolated sarcoplasmic reticulum (SR) vesicles to monovalent cations was studied using a stopped-flow fluorescence quenching technique that permits the measurement of ion fluxes on a millisecond time scale. Approximately 70% of the SR vesicles carry a cation conductance pathway mediating fluxes of Tl+, K+, Na+, and Li+, but not of choline. Both K+ and Na+ equilibrate faster than the 3-ms dead time of the apparatus and Li+ equilibrates in approximately 50 ms. These cation fluxes are reduced by a bis-guanidinium blocker of the SR K+ channel previously studied in planar bilayers. The remaining 30% of the vesicles are permeable to these cations on a time scale of seconds. We conclude that the SR K+ channel is present in a major fraction of vesicles and that its properties in the native membrane are similar to those found in planar bilayers. Moreover, the ion fluxes in fractionated SR vesicles suggest that the channels are distributed along the entire surface of the SR membrane, but in higher concentration in vesicles derived from the terminal cisternae region. From the measured rates of K+ movement, we calculate a conductance on the order of 10(-1) S/cm2 for the SR membrane in situ, which implies that this membrane cannot develop a potential of more than a few millivolts under physiological conditions.
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Facebook 
Reddit 
Technorati 
Twitter What's this?
This article has been cited by other articles:
|
|
 |
|
  P. C. Pape, K. Fenelon, C. R. H. Lamboley, and D. Stachura Role of calsequestrin evaluated from changes in free and total calcium concentrations in the sarcoplasmic reticulum of frog cut skeletal muscle fibres J. Physiol., May 15, 2007; 581(1): 319 - 367. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. Carmeliet Cardiac Ionic Currents and Acute Ischemia: From Channels to Arrhythmias Physiol Rev, July 1, 1999; 79(3): 917 - 1017. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. D. Buck and I. N. Pessah Mechanisms of delta -Hexachlorocyclohexane Toxicity: II. Evidence for Ca2+-Dependent K+-Selective Ionophore Activity J. Pharmacol. Exp. Ther., April 1, 1999; 289(1): 486 - 493. [Abstract] [Full Text]
|
|
|
|
 |
|
 R. Mejia-Alvarez, C. Kettlun, E. Rios, M. Stern, and M. Fill Unitary Ca2+ Current through Cardiac Ryanodine Receptor Channels under Quasi-Physiological Ionic Conditions J. Gen. Physiol., February 1, 1999; 113(2): 177 - 186. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. G Wood and J. I Gillespie In permeabilised endothelial cells IP3-induced Ca2+ release is dependent on the cytoplasmic concentration of monovalent cations Cardiovasc Res, January 1, 1998; 37(1): 263 - 270. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Sitsapesan, R. A.P. Montgomery, and A. J. Williams New Insights Into the Gating Mechanisms of Cardiac Ryanodine Receptors Revealed by Rapid Changes in Ligand Concentration Circ. Res., October 1, 1995; 77(4): 765 - 772. [Abstract] [Full Text]
|
|
|
|
 |
|
 E. Finch, T. Turner, and S. Goldin Calcium as a coagonist of inositol 1,4,5-trisphosphate-induced calcium release Science, April 19, 1991; 252(5004): 443 - 446. [Abstract] [PDF]
|
|
|
|
