Korean J Physiol Pharmacol.  2000 Jun;4(3):197-210.

Relationship between sarcoplasmic reticular calcium release and Na+-Ca2+ exchange in the rat myocardial contraction

• Kim EG
• Kim SJ
• Ko CM

Abstract

Suppressive role of Na+-Ca2+ exchange in myocardial tension generation was examined in the negative frequency-force relationship (FFR) of electric field stimulated left atria (LA) from postnatal developing rat heart and in the whole-cell clamped adult rat ventricular myocytes with high concentration of intracellular Ca2+ buffer (14 mM EGTA). LA twitch amplitudes, which were suppressed by cyclopiazonic acid in a postnatal age-dependent manner, elicited frequency-dependent and postnatal age-dependent enhancements after Na+-reduced, Ca2+-depleted (26 Na-0 Ca) buffer application. These enhancements were blocked by caffeine pretreatment with postnatal age-dependent intensities. In the isolated rat ventricular myocytes, stimulation with the voltage protocol roughly mimicked action potential generated a large inward current which was partially blocked by nifedipine or Na+ current inhibition. 0 Ca application suppressed the inward current by 39 +/- 4% while the current was further suppressed after 0 Na-0 Ca application by 53 +/- 3%. Caffeine increased this inward current by 44 +/- 3% in spite of 14 mM EGTA. Finally, the Na+ current-dependent fraction of the inward current was increased in a stimulation frequency-dependent manner. From these
results
, it is concluded that the Ca2+ exit-mode (forward-mode) Na+-Ca2+ exchange suppresses the LA tension by extruding Ca2+ out of the cell right after its release from sarcoplasmic reticulum (SR) in a frequency-dependent manner during contraction, resulting in the negative frequency-force relationship in the rat LA.

MeSH Terms

Action Potentials
Adult
Animals
Caffeine
Calcium*
Egtazic Acid
Heart
Humans
Muscle Cells
Myocardial Contraction*
Nifedipine
Rats*
Sarcoplasmic Reticulum
Caffeine
Calcium
Egtazic Acid
Nifedipine