|
|
|
|
|
|
|
||
The Journal of General Physiology, Vol 89, 921-958, Copyright © 1987 by The Rockefeller University Press
ARTICLES |
JL Kenyon and JL Sutko
We have used the two-microelectrode voltage-clamp technique to investigate the components of membrane current that contribute to the formation of the early part of the plateau phase of the action potential of calf cardiac Purkinje fibers. 3,4-Diaminopyridine (50 microM) reduced the net transient outward current elicited by depolarizations to potentials positive to -30 mV but had no consistent effect on contraction. We attribute this effect to the blockade of a voltage-activated transient potassium current component. Ryanodine (1 microM), an inhibitor of sarcoplasmic reticulum calcium release and intracellular calcium oscillations in Purkinje fibers (Sutko, J.L., and J.L. Kenyon. 1983. Journal of General Physiology. 82:385-404), had complex effects on membrane currents as it abolished phasic contractions. At early times during a depolarization (5-30 ms), ryanodine reduced the net outward current. We attribute this effect to the loss of a component of calcium-activated potassium current caused by the inhibition of sarcoplasmic reticulum calcium release and the intracellular calcium transient. At later times during a depolarization (50-200 ms), ryanodine increased the net outward current. This effect was not seen in low-sodium solutions and we could not observe a reversal potential over a voltage range of -100 to +75 mV. These data suggest that the effect of ryanodine on the late membrane current is attributable to the loss of sodium-calcium exchange current caused by the inhibition of sarcoplasmic reticulum calcium release and the intracellular calcium transient. Neither effect of ryanodine was dependent on chloride ions, which suggests that chloride ions do not carry the ryanodine-sensitive current components. Strontium (2.7 mM replacing calcium) and caffeine (10 mM), two other treatments that interfere with sarcoplasmic reticulum function, had effects in common with ryanodine. This supports the hypothesis that the effects of ryanodine may be attributed to the inhibition of sarcoplasmic reticulum calcium release.
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
|
|
 |
|
  M. A.G. van der Heyden, T. J.M. Wijnhoven, and T. Opthof Molecular aspects of adrenergic modulation of the transient outward current Cardiovasc Res, August 1, 2006; 71(3): 430 - 442. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Sun, D. Chartier, S. Nattel, and N. Leblanc Ca2+-activated Cl- current can be triggered by Na+ current-induced SR Ca2+ release in rabbit ventricle Am J Physiol Heart Circ Physiol, October 1, 1999; 277(4): H1467 - H1477. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Zhou, A. Jeron, B. London, X. Han, and G. Koren Characterization of a Slowly Inactivating Outward Current in Adult Mouse Ventricular Myocytes Circ. Res., October 19, 1998; 83(8): 806 - 814. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. L. Collier, P. C. Levesque, J. L. Kenyon, and J. R. Hume Unitary Cl- Channels Activated by Cytoplasmic Ca2+ in Canine Ventricular Myocytes Circ. Res., May 1, 1996; 78(5): 936 - 944. [Abstract] [Full Text]
|
|
|
|
 |
|
 L Barcenas-Ruiz, D. Beuckelmann, and W. Wier Sodium-calcium exchange in heart: membrane currents and changes in [Ca2+]i Science, December 18, 1987; 238(4834): 1720 - 1722. [Abstract] [PDF]
|
|
|
|
