Sr Ca-pump and Na/Ca exchange in relaxation of rabbit ventricular muscle

Bers, DM

doi:10.1016/0022-2828(88)90279-9

Cited by 5 publications

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“…Furthermore, the second RCC in this protocol was about the same as the first RCC when the cold and rewarming solutions were sodium-free and calcium-free (preventing Na-dependent calcium extrusion). 35 These results, along with the present study, suggest that under normal conditions the SR is responsible for most of relaxation (~75%), and Na-Ca exchange may be responsible for a smaller but substantial component (~25%). Of course, these estimates are approximate and may be expected to vary under different conditions.…”

Section: Sarcoplasmic Reticulum Calcium Pump and Na-ca Exchange In Ramentioning

confidence: 50%

“…This conclusion is directly supported by experiments where muscles were recooled 1 second after the rewarming relaxation was triggered. 35 The amplitude of this second RCC was 60-80% of that of the first RCC. This finding suggests that the SR reaccumulated most of the calcium released at the first RCC.…”

Section: Sarcoplasmic Reticulum Calcium Pump and Na-ca Exchange In Ramentioning

confidence: 99%

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Relaxation of rabbit ventricular muscle by Na-Ca exchange and sarcoplasmic reticulum calcium pump. Ryanodine and voltage sensitivity.

Bers

Bridge

1989

Circulation Research

162

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We studied relaxation during rapid rewanning of rabbit ventricular muscles that had been activated by rapid cooling. Rewanning from 1° to 30° C (in <0.5 second) activates mechanisms that contribute to the reduction of intracellular calcium concentration and thus relaxation (e.g., sarcoplasmic reticulum [SR] calcium pump and sarcolemmal Na-Ca exchange and calcium pump). Rapid rewanning in normal Tyrode's solution induces relaxation with a half-time (t^) of 217±14 msec (mean±SEM). During cold exposure, changing the superfusate to a sodiumfree, calcium-free medium with 2 mM CoCl 2 (to eliminate Na-Ca exchange) slightly slows relaxation upon rewanning in the same medium (t w =279±44 msec). Addition of 10 mM caffeine (which prevents SR calcium sequestration) to normal Tyrode's solution during cold superfusion slows relaxation somewhat more (t 1/2 =376±31 msec) than sodium-free, calciumfree solution. However, if both interventions are combined (sodium-free+caffeine) during the cold exposure and rewarming, the relaxation is greatly slowed (t 1/1 =2,580±810 msec). These results suggest that either the SR calcium pump or, to a lesser extent, sarcolemmal Na-Ca exchange can produce rapid relaxation, but if both systems are blocked, relaxation is very slow. If muscles are equilibrated with 500 nM ryanodine before cooling, relaxation upon rewarming is not greatly slowed (t 1/2 =266±37 msec) even if sodium-free, calcium-free solution is applied during the cold and rewarming phases (t l/2 =305±66 msec). This result suggests that ryanodine does not prevent the SR from accumulating calcium to induce relaxation. Relaxation in the presence of 10 mM caffeine appears to depend on a simple 3 : 1 Na-Ca exchange since relaxation is slowed by extracellular sodium reduction but stays constant with simultaneous reduction of extracellular sodium concentration and extracellular calcium concentration (where [Na] Received October 12, 1988; accepted January 13, 1989. occur, calcium must be removed from the myofilaments. At least three mechanisms are thought to be involved in reducing myoplasmic calcium: 1) the ATP-dependent SR calcium pump, 2) the sarcolemmal Na-Ca exchange, and 3) the sarcolemmal CaATPase pump. It is also possible that mitochondria contribute to relaxation by sequestering calcium 3 and other intracellular constituents that have very slow calcium-binding kinetics (relative to troponin C) could also be involved in relaxation. It is generally assumed that the SR calcium pump is the prtaeipaJ aecfeaeisfla responsible for relaxation. However, it is becoming increasingly dear that Na-Ca exchange can transport sufficient calcium rapidly enough to be involved in contraction and relaxation. 47 Here we investigate the relative contributions of the SR calcium pump and Na-Ca exchange in cardiac muscle relaxation.

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Section: Sarcoplasmic Reticulum Calcium Pump and Na-ca Exchange In Ramentioning

confidence: 50%

Section: Sarcoplasmic Reticulum Calcium Pump and Na-ca Exchange In Ramentioning

confidence: 99%

Relaxation of rabbit ventricular muscle by Na-Ca exchange and sarcoplasmic reticulum calcium pump. Ryanodine and voltage sensitivity.

Bers

Bridge

1989

Circulation Research

162

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Excitation‐Contraction Coupling in Heart Cells

Lederer

Berlin

Cohen

et al. 1990

Annals of the New York Academy of Sciences

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Experimental data do not support the idea that excitation-contraction coupling in heart muscle can be explained by a simple calcium-induced calcium release mechanism alone or a simple voltage-dependent calcium release mechanism alone. Our data on excitation-contraction coupling combined with the results of others suggest the need to either develop more complex and more sophisticated single-mechanism models, or to establish dual-control models.

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Species Differences and the Role of Sodium‐Calcium Exchange in Cardiac Muscle Relaxation^a

Bers

1991

Annals of the New York Academy of Sciences

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During normal relaxation in rabbit, guinea-pig, and rat ventricular muscle, the Na-Ca exchange system competes with the SR Ca pump, with the former being responsible for about 20-30% of the Ca removal from the cytoplasm. Ca extrusion via Na-Ca exchange is Em-sensitive, whereas Ca uptake by the SR is not. Neither the sarcolemmal Ca-ATPase pump nor mitochondrial Ca uptake appear to contribute significantly to the decline of [Ca]i during relaxation. Furthermore, the diastolic efflux of Ca from cardiac muscle cells appears to be primarily attributable to Na-Ca exchange and not the sarcolemmal Ca-ATPase pump. In rabbit ventricle Ca entry via Na-Ca exchange is favored thermodynamically during much of a normal twitch contraction and Ca extrusion occurs primarily between beats. In rat ventricle Ca efflux via Na-Ca exchange occurs during the contraction and net Ca influx may occur between beats. This fundamental difference in Ca fluxes during the cardiac cycle in rat versus rabbit ventricle may be a simple consequence of the shorter action potential duration and higher aNai in rat ventricle (due to the effects of Em and [Na] and [Ca] gradients on Na-Ca exchange).

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Sr Ca-pump and Na/Ca exchange in relaxation of rabbit ventricular muscle

Cited by 5 publications

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Relaxation of rabbit ventricular muscle by Na-Ca exchange and sarcoplasmic reticulum calcium pump. Ryanodine and voltage sensitivity.

Relaxation of rabbit ventricular muscle by Na-Ca exchange and sarcoplasmic reticulum calcium pump. Ryanodine and voltage sensitivity.

Excitation‐Contraction Coupling in Heart Cells

Species Differences and the Role of Sodium‐Calcium Exchange in Cardiac Muscle Relaxation^a

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Sr Ca-pump and Na/Ca exchange in relaxation of rabbit ventricular muscle

Cited by 5 publications

References 0 publications

Relaxation of rabbit ventricular muscle by Na-Ca exchange and sarcoplasmic reticulum calcium pump. Ryanodine and voltage sensitivity.

Relaxation of rabbit ventricular muscle by Na-Ca exchange and sarcoplasmic reticulum calcium pump. Ryanodine and voltage sensitivity.

Excitation‐Contraction Coupling in Heart Cells

Species Differences and the Role of Sodium‐Calcium Exchange in Cardiac Muscle Relaxationa

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Species Differences and the Role of Sodium‐Calcium Exchange in Cardiac Muscle Relaxation^a