Relaxation in rabbit and rat cardiac cells: species-dependent differences in cellular mechanisms

• Published in: The Journal of physiology Vol. 476; no. 2; pp. 279 - 293
• Main Authors: Bassani, J W, Bassani, R A, Bers, D M
• Format: Journal Article
• Language: English
• Published: England The Physiological Society 15-04-1994
• Subjects: Action Potentials - physiology; Animals; Caffeine - pharmacology; Calcium - metabolism; Calcium-Transporting ATPases - metabolism; Carrier Proteins - physiology; Electric Stimulation; Fluorescence; Heart - drug effects; Heart - physiology; In Vitro Techniques; Male; Myocardial Contraction - drug effects; Myocardial Contraction - physiology; Myocardium - cytology; Myocardium - enzymology; Rabbits; Rats; Rats, Sprague-Dawley; Sarcoplasmic Reticulum - enzymology; Sodium - metabolism; Sodium-Calcium Exchanger; Species Specificity
• ISSN: 0022-3751; 1469-7793
• DOI: 10.1113/jphysiol.1994.sp020130

The roles of the sarcoplasmic reticulum (SR) Ca(2+)-ATPase and Na(+)-Ca2+ exchange in Ca2+ removal from cytosol were compared
in isolated rabbit and rat ventricular myocytes during caffeine contractures and electrically stimulated twitches. Cell shortening
and intracellular calcium concentration ([Ca2+]i) were measured in indo-1-loaded cells. Na(+)-Ca2+ exchange was inhibited
by replacement of external Na+ by Li+. To avoid net changes in cell or SR Ca2+ load during a twitch in 0 Na+ solution, intracellular
Na+ (Na+i) was depleted using a long pre-perfusion with 0 Na+, 0 Ca2+ solution. SR Ca2+ accumulation was inhibited by caffeine
or thapsigargin (TG). Relaxation of steady-state twitches was 2-fold faster in rat than in rabbit (before and after Na+i depletion).
In contrast, caffeine contractures (where SR Ca2+ accumulation is inhibited), relaxed faster in rabbit cells. Removal of external
Na+ increased the half-time for relaxation of caffeine contractures 15- and 5-fold in rabbit and rat myocytes respectively
(and increased contracture amplitude in rabbit cells only). The time course of relaxation in 0 Na+, 0 Ca2+ solution was similar
in the two species. Inhibition of the Na(+)-Ca2+ exchange during a twitch increased the [Ca2+]i transient amplitude (delta[Ca2+]i)
by 50% and the time constant of [Ca2+]i decline (tau) by 45% in rabbit myocytes. A smaller increase in tau (20%) and no change
in delta[Ca2+]i were observed in rat cells in 0 Na+ solution. [Ca2+]i transients remained more rapid in rat cells. Inhibition
of the SR Ca(2+)-ATPase during a twitch enhanced delta[Ca2+]i by 25% in both species. The increase in tau after TG exposure
was greater in rat (9-fold) than in rabbit myocytes (2-fold), which caused [Ca2+]i decline to be 70% slower in rat compared
with rabbit cells. The time course of [Ca2+]i decline during twitch in TG-treated cells was similar to that during caffeine
application in control cells. Combined inhibition of these Ca2+ transport systems markedly slowed the time course of [Ca2+]i
decline, so that tau was virtually the same in both species and comparable to that during caffeine application in 0 Na+, 0
Ca2+ solution. Thus, the combined participation of slow Ca2+ transport mechanisms (mitochondrial Ca2+ uptake and sarcolemmal
Ca(2+)-ATPase) is similar in these species. We conclude that during the decline of the [Ca2+]i transient, the Na(+)-Ca2+ exchange
is about 2- to 3-fold faster in rabbit than in rat, whereas the SR Ca(2+)-ATPase is 2- to 3-fold faster in the rat.