PMID- 8046643 OWN - NLM STAT- MEDLINE DCOM- 19940901 LR - 20191210 IS - 0022-3751 (Print) IS - 1469-7793 (Electronic) IS - 0022-3751 (Linking) VI - 476 IP - 2 DP - 1994 Apr 15 TI - Relaxation in rabbit and rat cardiac cells: species-dependent differences in cellular mechanisms. PG - 279-93 AB - 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.(ABSTRACT TRUNCATED AT 400 WORDS) FAU - Bassani, J W AU - Bassani JW AD - Department of Physiology, Loyola University School of Medicine, Maywood, IL 60153. FAU - Bassani, R A AU - Bassani RA FAU - Bers, D M AU - Bers DM LA - eng GR - HL-30077/HL/NHLBI NIH HHS/United States PT - Comparative Study PT - Journal Article PT - Research Support, U.S. Gov't, P.H.S. PL - England TA - J Physiol JT - The Journal of physiology JID - 0266262 RN - 0 (Carrier Proteins) RN - 0 (Sodium-Calcium Exchanger) RN - 3G6A5W338E (Caffeine) RN - 9NEZ333N27 (Sodium) RN - EC 7.2.2.10 (Calcium-Transporting ATPases) RN - SY7Q814VUP (Calcium) SB - IM MH - Action Potentials/physiology MH - Animals MH - Caffeine/pharmacology MH - Calcium/metabolism MH - Calcium-Transporting ATPases/metabolism MH - Carrier Proteins/physiology MH - Electric Stimulation MH - Fluorescence MH - Heart/drug effects/*physiology MH - In Vitro Techniques MH - Male MH - Myocardial Contraction/drug effects/*physiology MH - Myocardium/*cytology/enzymology MH - Rabbits MH - Rats MH - Rats, Sprague-Dawley MH - Sarcoplasmic Reticulum/enzymology MH - Sodium/metabolism MH - Sodium-Calcium Exchanger MH - Species Specificity PMC - PMC1160440 EDAT- 1994/04/15 00:00 MHDA- 1994/04/15 00:01 PMCR- 1994/04/15 CRDT- 1994/04/15 00:00 PHST- 1994/04/15 00:00 [pubmed] PHST- 1994/04/15 00:01 [medline] PHST- 1994/04/15 00:00 [entrez] PHST- 1994/04/15 00:00 [pmc-release] AID - 10.1113/jphysiol.1994.sp020130 [doi] PST - ppublish SO - J Physiol. 1994 Apr 15;476(2):279-93. doi: 10.1113/jphysiol.1994.sp020130.