The Accumulation of Calcium Ions by Sarcotubular Vesicles

Carsten, Mary E.; Mommaerts, W. F. H. M.

doi:10.1085/jgp.48.2.183

Cited by 82 publications

(21 citation statements)

References 49 publications

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“…A. GRAHAM AAND J. F. LAMB some evidence that in hypodynamia the Ca uptake is depressed and may be restored by ouabain (Gertz et al 1967). It has also been noted that if the microsomal Ca uptake from skeletal muscle is depressed by caffeine, 3'5'-AMP will restore it (Carsten & Mommaerts, 1964). We think it possible that our store is similar to these sarcotubular elements, i.e.…”

Section: Discussionmentioning

confidence: 82%

The effect of adrenaline on the tension developed in contractures and twitches of the ventricle of the frog

Graham¹,

Lamb²

1968

The Journal of Physiology

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SUMMARY1. The effect of adrenaline on contracture and twitch tension in frog's ventricle has been examined, using the superfused preparation.2. In 1 mM-Ca Ringer, contractures induced with excess KCl concentrations from 50 to 200 mm, are reduced by 1 x 106 g/ml. adrenaline to an average of 0*62 of control values, in marked contrast to the well known positive inotropic effect of adrenaline on the heart twitch. This effect of adrenaline is directly dose dependent. Increasing [Ca]. diminishes the effect of adrenaline on contracture tension, and on the twitch tension.3. Adrenaline has a significantly greater effect on the KCl contracture tension than noradrenaline or isoprenaline.4. In 1 mM-Ca Ringer, Na-free contractures are reduced to 0-72 of controls by 1 x 106 g/ml. adrenaline. Adrenaline also significantly reduces tension in contractures induced by 50 c/s alternating current.5. The action of adrenaline on contracture tension is largely complete in 1-2 min at various rates of stimulation and calcium concentrations. A similar time course has been found for the effect of adrenaline on membrane potential.6. Pronethalol blocks the action of adrenaline on both twitch and contracture. The action on the contracture can also be blocked by ouabain (1 X 10-5 M), and exposure of the tissue to K-free or Na-free Ringer solution.7. Adrenaline hyperpolarizes the membrane potential with a range of [K]o from 0 to 200 mm. This effect is blocked by pronethalol and ouabain. After exposure to ouabain, adrenaline causes a significant decrease in the membrane potential. This may be due to an increase in the sodium permeability.8. At low values of the [Ca]/[Na]2 ratio, adrenaline takes a relatively constant number of beats for full action, but at high values of the ratio the development of full effect is largely time dependent.

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Section: Discussionmentioning

confidence: 82%

The effect of adrenaline on the tension developed in contractures and twitches of the ventricle of the frog

Graham¹,

Lamb²

1968

The Journal of Physiology

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“…Evidence that such a sequence of events can follow inhibition of the calcium pump is suggested by the experiments of Foulks and Perry (17). These investigators found that sodium pentobarbital, a drug known to inhibit the calcium pump of skeletal muscle (18,19), produces an initial increase in contractility followed by an inhibition of contractility. Implicit in the above discussion is the idea of competitive pathways for the metabolism of calcium.…”

Section: Discussionmentioning

confidence: 99%

Activity of the Vesicular Calcium Pump in the Spontaneously Failing Heart-Lung Preparation

Gertz

Heß

Lain

et al. 1967

Circulation Research

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The in vitro calcium uptake activity has been examined in fragments of sarcoplasmic reticulum, i.e. vesicles, obtained from hearts spontaneously failing in the canine heart-lung preparation. The rate of uptake was found to be less than that observed for vesicles from control hearts. If the vesicles were prepared from a failed heart that had been treated in vivo with ouabain, then the rate of calcium uptake was normal. In vitro additions of ouabain increased the rate of calcium uptake only with vesicles prepared from failing hearts. This effect of ouabain on calcium uptake by vesicles appears, therefore, to be specific for the defect causing depression of calcium uptake. No evidence could be found that the depression of calcium uptake is due to uncoupling of the pump adenosine triphosphatase. Calcium uptake and adenosine triphosphatase activity were found to be proportionately depressed in the failing heart and proportionately restored by ouabain.ADDITIONAL KEY WORDS adenosine triphosphatase sarcoplasmic reticulurn excitation-contraction coupling ouabain heart failure calcium uptake anesthetized dogs• The excitation-contraction (1, 2) coupling mechanism has long been suspected (3, 4) to be involved in heart failure. Ignorance concerning the mechanism of excitation-contraction coupling and inability to evaluate its state has, however, heretofore prevented any direct assessment of this possibility. Our present understanding of the importance of the sarcotubular calcium pump (5-8) in the operation of excitation-contraction coupling and our ability to isolate and investigate this pump has recently made it possible to determine if some abnormality of it is associated with heart failure. Briggs, Gertz and Hess, in a recent report (5), have suggested that the heart From the

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“…Oligomycin is a powerful blocking agent of mitochondrial-oxidative phosphorylation, but its action on calcium transport by isolated sarcoplasmic reticulum occurs only at high concentrations (Carsten & Mommaerts, 1964). In the heart the application of oligomycin at concentrations of between 10-6 and 10-5 g ml.-' results in a slowing of the spontaneous relaxation of the potassium contracture only after at least 20 min exposure, to the chemical.…”

Section: Resultsmentioning

confidence: 99%

“…Antimycin A, which blocks mitochondrial respiration based phosphorylation by interfering with the cytochrome system, potentiates calcium ion uptake in cardiac sarcoplasmic microsomes (Carsten & Mommaerts, 1964).…”

Section: Resultsmentioning

confidence: 99%

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The effects of temperature and metabolic inhibitors on the spontaneous relaxation of the potassium contracture of the heart of the frog Rana pipiens

Chapman¹

1973

The Journal of Physiology

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SUMMAARY1. The spontaneous relaxation of the potassium contracture and the relaxation induced by the removal of extracellular calcium or the restoration of the original potassium concentration, in the frog heart, show a strong dependence on temperature.2. The energy of activation of the later exponential phase of the spontaneous relaxation is 1043 kcal mole-1, a value close to that reported for the binding of calcium ions by isolated sarcoplasmic reticulum, but larger than that for the calcium efflux from mammalian heart.3. The use ofmetabolic inhibitors shows that relaxation can be sustained when glycolysis is poisoned, but the disruption of oxidative phosphorylation slows relaxation.4. Poisoning of both glycolysis and oxidative phosphorylation blocks all but the small initial part of the spontaneous relaxation of the potassium contracture and also interferes with relaxation induced by other means.5. The results are considered to favour the existence, in frog heart, of an active intracellular relaxing system which uses ATP as its substrate to lower the sarcoplasmic calcium concentration. This system is likely to be the sarcoplasmic reticulum but the mitochondria could also be involved.

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The Accumulation of Calcium Ions by Sarcotubular Vesicles

Cited by 82 publications

References 49 publications

The effect of adrenaline on the tension developed in contractures and twitches of the ventricle of the frog

The effect of adrenaline on the tension developed in contractures and twitches of the ventricle of the frog

Activity of the Vesicular Calcium Pump in the Spontaneously Failing Heart-Lung Preparation

The effects of temperature and metabolic inhibitors on the spontaneous relaxation of the potassium contracture of the heart of the frog Rana pipiens

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