scholarly journals Relationships between the sarcoplasmic reticulum and sarcolemmal calcium transport revealed by rapidly cooling rabbit ventricular muscle.

1986 ◽  
Vol 88 (4) ◽  
pp. 437-473 ◽  
Author(s):  
J H Bridge
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Calcium Transport ◽  
Fourier Spectrum ◽  
Papillary Muscles ◽  
Ventricular Muscle ◽  
Relative Index ◽  
Voltage Dependent ◽  
Intracellular Ca ◽  
Muscle Cooling ◽  
Rabbit Ventricular Muscle

Rabbit right ventricular papillary muscles were cooled from 30 to approximately 1 degree C immediately after discontinuing electrical stimulation (0.5 Hz). This produced a contracture that was 30-50% of the preceding twitch magnitude and required 20-30 s to develop. The contractures were identical in cooling solutions with normal (144 mM) or low (2.0 mM) Na. They were therefore not Na-withdrawal contractures. Contracture activation was considerably slower than muscle cooling (approximately 2.5 s to cool below 2 degrees C). Cooling contractures were suppressed by caffeine treatment (10.0 mM). Rapid cooling did not cause sufficient membrane depolarization (16.5 +/- 1.2 mV after 30 s of cooling) to produce either a voltage-dependent activation of contracture or a gated entry of Ca from the extracellular space. Contractures induced by treating resting muscles with 5 X 10(-5) M strophanthidin at 30 degrees C exhibited pronounced tension noise. The Fourier spectrum of this noise revealed a periodic component (2-3 Hz) that disappeared when the muscle was cooled. Cooling contractures decayed with rest (t1/2 = 71.0 +/- 9.3 s). This decay accelerated in the presence of 10.0 mM caffeine and was prevented and to some extent reversed when extracellular Na was reduced to 2.0 mM. 20 min of rest resulted in a net decline in intracellular Ca content of 1.29 +/- 0.38 mmol/kg dry wt. I infer that cooling contractures are principally activated by Ca from the sarcoplasmic reticulum (SR). The properties of these contractures suggest that they may provide a convenient relative index of the availability of SR Ca for contraction. The rest decay of cooling contractures (and hence the decay in the availability of activating Ca) is consistent with the measured loss in analytic Ca during rest. The results suggest that contraction in heart muscle can be regulated by an interaction between sarcolemmal and SR Ca transport.

Ryanodine and the calcium content of cardiac SR assessed by caffeine and rapid cooling contractures

1987 ◽  
Vol 253 (3) ◽  
pp. C408-C415 ◽  
Author(s):  
D. M. Bers
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Calcium Content ◽  
Ventricular Muscle ◽  
Free Medium ◽  
Rapid Cooling ◽  
Relative Index ◽  
Tension Level ◽  
Resting Tension ◽  
Rabbit Ventricular Muscle ◽  
Caffeine Contractures

The ability of rabbit ventricular muscle sarcoplasmic reticulum (SR) to accumulate and retain Ca during Na-free perfusion was assessed using caffeine contractures and rapid cooling contractures (RCC). Muscles were exposed to a Na-free medium for 15 min, during which time a transient contracture developed and relaxed back to the resting tension level. Muscles were then either exposed to 20 mM caffeine or rapidly cooled to less than 5 degrees C, both of which produced large contractures. The magnitudes of those contractures are believed to be a relative index of SR Ca content. Reduction of extracellular [Ca] from 2 to 0.2 mM did not significantly alter the magnitude of either Na-free caffeine contractures or RCC. These are not the maximum contractures that can be obtained. The possibility that low extracellular [Ca] ([Ca]o) may increase passive Ca permeability is suggested in explanation of this effect. After equilibration with 100 nM ryanodine, both Na-free caffeine contractures and RCC are virtually eliminated. This suggests that even if the SR could accumulate Ca during the initial Na-free exposure in the presence of ryanodine, it could not retain that Ca in Na-free medium. It is proposed that the sarcolemmal Ca pump can extrude Ca from the cells at a rate sufficient to deplete the ryanodine-treated SR. When removal of Na was accompanied by increase of [K]o (to 12, 20, or 30 mM), the Na-free RCC were enhanced. Increasing [K]o during Na-free superfusion in the presence of ryanodine resulted in demonstrable RCC that were graded with [K] and completely suppressed by nifedipine.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of sevoflurane on the contractility of ferret ventricular myocardium

2000 ◽  
Vol 89 (5) ◽  
pp. 1778-1786 ◽  
Author(s):  
Anna E. Bartunek ◽  
Philippe R. Housmans
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Right Ventricular ◽  
Ventricular Myocardium ◽  
Papillary Muscles ◽  
Depressant Effect ◽  
Intracellular Ca ◽  
Mild Stimulation ◽  
Equal Amplitude ◽  
Stimulation Of

Isotonic and isometric variables of contractility and relaxation of isolated ferret right ventricular papillary muscles were measured before and during exposure to incremental concentrations of sevoflurane (0–4.9% vol/vol) (30°C) ( n = 9). In a second group of muscles ( n = 8), effects of sevoflurane were compared with those of low [Ca2+]o (0.45–2.25 mM in steps of 0.45 mM). Sevoflurane caused a reversible concentration-dependent decrease in contractility (ED50 of developed force 4.6 ± 0.9% vol/vol). When compared with twitches of equal amplitude in low extracellular Ca2+ concentration, sevoflurane accelerated both isometric and isotonic relaxation. The myocardial depressant effect of sevoflurane is less than that of isoflurane and results mainly from a decrease of intracellular Ca2+ availability. The abbreviated isometric relaxation likely reflects a decrease in Ca2+ sensitivity and the faster isotonic relaxation may reflect a mild stimulation of Ca2+ uptake by the sarcoplasmic reticulum.

The mechanism of ryanodine action in rabbit ventricular muscle evaluated with Ca-selective microelectrodes and rapid cooling contractures

1987 ◽  
Vol 65 (4) ◽  
pp. 610-618 ◽  
Author(s):  
Donald M. Bers ◽  
John H. B. Bridge ◽  
Kenneth T. MacLeod
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Extracellular Space ◽  
Repetitive Stimulation ◽  
Ventricular Muscle ◽  
Half Time ◽  
Rapid Cooling ◽  
Ca Uptake ◽  
Rabbit Ventricular Muscle ◽  
Independent Assay ◽  
Cellular Ca

Cellular Ca uptake and efflux in rabbit ventricular muscle was measured using double-barreled Ca microelectrodes in the extracellular space. When repetitive stimulation was stopped there was a slow loss of cellular Ca. Upon resumption of stimulation Ca was taken up by the cells. These Ca movements are thought to represent the loss of Ca from the sarcoplasmic reticulum and the cell during rest and the refilling of the sarcoplasmic reticulum during stimulation. Ryanodine (100 nM) greatly enhanced both the efflux of Ca during rest and the uptake of Ca induced by stimulation. These results are consistent with the conclusions drawn below, but they are dependent upon the interpretation that these extracellular Ca depletions are indicative of sarcoplasmic reticulum Ca movements. To examine further this process, contractures induced by rapid cooling to 0 °C were used as an independent assay of sarcoplasmic reticulum Ca content. These rapid cooling contractures were smaller after longer rest intervals (declining with a half time of 1.5 min). In the presence of ryanodine, the rapid cooling contracture immediately after a contraction was greater than that seen under control conditions. However, in the presence of ryanodine these rapid cooling contractures decline as a function of rest duration with a half time of about 1 s. These results suggest that in the presence of ryanodine the sarcoplasmic reticulum can still take up Ca, but that it also loses this Ca very rapidly at the onset of rest. Caffeine (20 mM) inhibits both the extracellular Ca depletions and the rapid cooling contractures that are attributed to the sarcoplasmic reticulum Ca content changes (in the presence or absence of ryanodine). These results suggest the following two actions of ryanodine: (i) inhibition of sarcoplasmic reticulum Ca release into the cytoplasm upon activation, and (ii) enhancement of Ca loss from the sarcoplasmic reticulum upon the termination of stimulation and extrusion from the cell without activation of appreciable tension.

Effects of rest duration and ryanodine on changes of extracellular [Ca] in cardiac muscle from rabbits

1987 ◽  
Vol 253 (3) ◽  
pp. C398-C407 ◽  
Author(s):  
K. T. MacLeod ◽  
D. M. Bers
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Cardiac Muscle ◽  
Extracellular Space ◽  
Ventricular Muscle ◽  
Rest Interval ◽  
Continuous Stimulation ◽  
Rabbit Ventricular Muscle ◽  
Interpretive Framework ◽  
Rest Intervals

Cumulative depletions of extracellular Ca were measured using double-barreled Ca-sensitive microelectrodes in the extracellular space of rabbit ventricular muscle. Depletions were produced by 1-Hz stimulation after rest intervals of 10 s to 10 min. With longer rest intervals, depletion size increased while the first postrest contraction decreased in a reciprocal manner. The depletions may represent refilling of sarcoplasmic reticulum (SR) Ca stores that have become partially depleted of Ca during the rest. Within this interpretive framework, the longer the rest interval the lower the SR Ca content, so the SR is then capable of taking up larger amounts of Ca. This may be related to the rest decay of tension of the first postrest beat, since this is thought to be SR dependent. Ryanodine (1 microM) increased the size of the depletions after short rest intervals (less than 2 min) but not after longer (greater than or equal to 2 min) intervals. Ryanodine also increased the rate of Ca loss from the cell on cessation of stimulation. This increased rate of Ca loss with ryanodine may deplete the SR of Ca such that more Ca can be taken up during subsequent stimulation than in untreated muscles. Thus cumulative depletions after short rest intervals are enhanced by ryanodine. When a Ca load was produced during 1) quiescence [by removal of extracellular Na (Nao)] or 2) continuous stimulation (in the presence of 3 microM acetylstrophanthidin), addition of ryanodine (5-10 microM) did not produce any apparent Ca loss. Caffeine (10 mM), added after ryanodine, induced contractures accompanied by Ca efflux, implying there was Ca in the SR after ryanodine exposure. The results of other investigators have suggested that ryanodine may inhibit cardiac SR Ca release. The present study suggests that ryanodine also enhances the loss of cellular (and probably SR) Ca on cessation of stimulation but not when applied during continuous stimulation or quiescence.

Temperature dependence of myofilament Ca sensitivity of rat, guinea pig, and frog ventricular muscle

1990 ◽  
Vol 258 (2) ◽  
pp. C274-C281 ◽  
Author(s):  
S. M. Harrison ◽  
D. M. Bers
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Guinea Pig ◽  
Temperature Dependence ◽  
Cardiac Muscle ◽  
Ventricular Muscle ◽  
Rapid Cooling ◽  
Intracellular Ca ◽  
Ca Sensitivity

Cooling the superfusate of intact ventricular muscle, from 30 degrees C to below 4 degrees C in less than 2 s, leads to contractures thought to reflect the amount of Ca available for release from the sarcoplasmic reticulum (SR). On rewarming, tension transiently increases in guinea pig and rat ventricular muscle. It has been proposed that this rewarming tension spike reflects changes in myofilament Ca sensitivity and maximum Ca-activated force (Cmax) associated with rewarming. There are differences in intracellular Ca regulation among cardiac muscle preparations. Some characteristics of rapid-cooling contractures (e.g., the magnitude of the rewarming spike) also differ between species. Therefore, the Ca sensitivity of skinned ventricular muscle from the rat, guinea pig, and frog was determined at 29 (22 degrees C for frog ventricular preparations), 8, and 1 degrees C. The results show that cooling rat and guinea pig ventricular muscle from 29 to 1 degrees C shifts the pCa vs. tension relationship toward higher [Ca2+] by 0.65 and 0.55 pCa units, respectively. Cooling to 1 degrees C also reduced Cmax to 3.3 and 7.8% of that at 29 degrees C in rat and guinea pig ventricular muscle, respectively. Similar results were found for frog ventricular muscle, in which cooling from 22 to 1 degrees C reduced Ca sensitivity by 0.6 pCa units and Cmax to 45.7% of its value at 22 degrees C.(ABSTRACT TRUNCATED AT 250 WORDS)

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