HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 286/2/C330    most recent 00272.2003v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (16) Citing Articles via Google Scholar Google Scholar Articles by Zahradníková, A. Articles by Zahradník, I. Search for Related Content PubMed PubMed Citation Articles by Zahradníková, A. Articles by Zahradník, I.

MEMBRANE TRANSPORTERS, ION CHANNELS, AND PUMPS

Activation of calcium release assessed by calcium release-induced inactivation of calcium current in rat cardiac myocytes

¹Institute of Molecular Physiology and Genetics, Slovak Academy of Sciences, 833 34 Bratislava, Slovakia; and ²Department of Physiology, Texas Tech University Health Sciences Center, Lubbock, Texas 79430

Submitted 30 June 2003 ; accepted in final form 29 September 2003

In mammalian cardiac myocytes, calcium released into the dyadic space rapidly inactivates calcium current (I_Ca). We used this Ca²⁺ release-dependent inactivation (RDI) of I_Ca as a local probe of sarcoplasmic reticulum Ca²⁺ release activation. In whole cell patch-clamped rat ventricular myocytes, Ca²⁺ entry induced by short prepulses from —50 mV to positive voltages caused suppression of peak I_Ca during a test pulse. The negative correlation between peak I_Ca suppression and I_Ca inactivation during the test pulse indicated that RDI evoked by the prepulse affected only calcium channels in those dyads in which calcium release was activated. Ca²⁺ ions injected during the prepulse and during the subsequent tail current suppressed peak I_Ca in the test pulse to a different extent. Quantitative analysis indicated that equal Ca²⁺ charge was 3.5 times less effective in inducing release when entering during the prepulse than when entering during the tail. Tail Ca²⁺ charge injected by the first voltage-dependent calcium channel (DHPR) openings was three times less effective than that injected by DHPR reopenings. These findings suggest that calcium release activation can be profoundly influenced by the recent history of L-type Ca²⁺ channel activity due to potentiation of ryanodine receptors (RyRs) by previous calcium influx. This conclusion was confirmed at the level of single RyRs in planar lipid bilayers: using flash photolysis of the calcium cage NP-EGTA to generate two sequential calcium stimuli, we showed that RyR activation in response to the second stimulus was four times higher than that in response to the first stimulus.

excitation-contraction coupling

This article has been cited by other articles:

				E. Polakova, A. Zahradnikova Jr, J. Pavelkova, I. Zahradnik, and A. Zahradnikova Local calcium release activation by DHPR calcium channel openings in rat cardiac myocytes J. Physiol., August 15, 2008; 586(16): 3839 - 3854. [Abstract] [Full Text] [PDF]

				A. Zahradnikova Jr, E. Polakova, I. Zahradnik, and A. Zahradnikova Kinetics of calcium spikes in rat cardiac myocytes J. Physiol., February 1, 2007; 578(3): 677 - 691. [Abstract] [Full Text] [PDF]

				I. Zahradnik, S. Gyorke, and A. Zahradnikova Calcium Activation of Ryanodine Receptor Channels--Reconciling RyR Gating Models with Tetrameric Channel Structure J. Gen. Physiol., October 31, 2005; 126(5): 515 - 527. [Abstract] [Full Text] [PDF]

				S. Viatchenko-Karpinski, D. Terentyev, L. A. Jenkins, L. O. Lutherer, and S. Gyorke Synergistic interactions between Ca2+ entries through L-type Ca2+ channels and Na+-Ca2+ exchanger in normal and failing rat heart J. Physiol., September 1, 2005; 567(2): 493 - 504. [Abstract] [Full Text] [PDF]