Action of caffeine on calcium transport by isolated fractions of myofibrils, mitochondria, and sarcoplasmic reticulum from rabbit heart.

Blayney, Lynda Mary; Thomas, H. R.; Muir, John; Henderson, A R

doi:10.1161/01.res.43.4.520

Cited by 76 publications

(34 citation statements)

References 34 publications

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“…This increase of cyclic AMP might lead to protein-kinase-catalyzed phosphorylation of phospholambam and an increased calcium uptake by the SR calcium pump (Hicks et al, 1979;Tada et al, 1979). Caffeine, however, only increases the myofibrillar ATPase activity at a concentration of 20 mM (Blayney et al, 1978). Our current finding that theophylline, a more potent phosphodiesterase inhibitor (Goodman and Gilman, 1970), produces exactly the same reversal as does caffeine would indicate that this phosphodiesterase inhibition may not be the primary controlling factor.…”

Section: Discussionmentioning

confidence: 61%

“…No consistent increase of resting force was found. (3) Caffeine increases the calcium permeability of the sarcolemma (Nayler, 1963;Blinks et al, 1972;Kavaler et al, 1978) and vesicles (Blayney et al, 1978). This increased permeability and potentially increased calcium efflux from the SR depends on the relative internal and external calcium concentrations (Katz 597 et al, 1977).…”

Section: Discussionmentioning

confidence: 99%

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Caffeine reversal of length-dependent changes in myocardial contractile state in the cat.

Chuck¹,

Parmley²

1980

Circulation Research

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SUMMARY The present study evaluated potential mechanisms for the slow length-dependent change in myocardial contractile state. Using 40 isolated right ventricular cat papillary muscles, we found that 10 mM caffeine reversed the subsequent slow change in myocardial performance following a change in muscle length. Since caffeine acts both at the sarcolemma and the sarcoplasmic reticulum, we attenuated the sarcolemmal influx of calcium with verapamil, manganese, and low external calcium concentration. None of these interventions altered the caffeine reversal of the length-dependent effect. It thus appears that the length-dependent alteration of contractile state is of intracellular origin, and probably related to altered calcium handling by the sarcoplasmic reticulum. Circ Res 47: 592-598, 1980 THE relationship between muscle length and cardiac performance has been described by the FrankStarling relationship. After an increase in end-diastolic fiber length along the ascending limb of this relationship, there is an increase in cardiac performance. At any given length, positive inotropic agents can further increase cardiac performance. Thus, the traditional view was that these two mechanisms for altering cardiac performance were independent of each other. The Frank-Starling relationship was explained by a variation in the number of crossbridges formed between the contractile proteins (Gordon et al., 1966). The positive inotropic response was explained by an increase in the rate of interaction of these cross-bridges (Katz, 1970).Contrary to the traditional belief that these two mechanisms for altering cardiac performance were separate from one another, we reported a slow length-dependent change in myocardial contractile state (Parmley and Chuck, 1973). In isolated cat papillary muscles, the immediate response to an increase of muscle length was followed by a slow additional increase in performance. Thus, in addition to the instantaneous length, the length history becomes an important determinant of the "FrankStarling" response. Subsequent studies have suggested that the immediate increase in force along the ascending limb is due not so much to myofilament and cross-bridge overlap, but to a lengthdependent alteration in the amount of calcium activating these cross-bridges (Allen et al., 1974;Jewell, 1977;Lakatta and Jewell, 1977;Fabiato and Fabiato, 1975 Received June 4, 1979; accepted for publication May 27,1980. tions the traditional separation between alterations in performance due to length and contractility. In our early attempts to identify a mechanism for the slow time-dependent coupling between muscle length and contractile state, we ruled out crosssectional area, release of stored catecholamines, temperature effects (24°-37°C), or series viscous elements as mechanisms for this observation (Parmley and Chuck, 1973). We did find, however, that varying the external calcium concentration changed the magnitude of the slow response, suggesting a calcium-mediated mechanism. In this paper, we report additional s...

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Section: Discussionmentioning

confidence: 61%

Section: Discussionmentioning

confidence: 99%

Caffeine reversal of length-dependent changes in myocardial contractile state in the cat.

Chuck¹,

Parmley²

1980

Circulation Research

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“…The observed effects of caffeine and ryanodine are supportive of the interpretation that Pi is the result of sarcoplasmic reticulum release of activator cation. The concentration of caffeine used in this study (1 ITIM) significantly reduces both the rate of Ca accumulation and the net steady state amount of Ca accumulated by fragmented sarcoplasmic reticulum isolated from rabbit heart (Blayney et al, 1978 marked reduction of Pi by caffeine may therefore be related to this action of caffeine rather than the membrane effects of the drug which tend to increase contractility (Blinks et al, 1972;Kavaler et al, 1978). Since caffeine has multiple actions, it was considered desirable to test the effects of another inhibitor of divalent cation release from the sarcoplasmic reticulum.…”

Section: Site Of Cation Causing Pimentioning

confidence: 83%

Mechanism of biphasic contractions in strontium-treated ventricular muscle.

King¹,

Böse²

1983

Circulation Research

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SUMMARY. Biphasic contractions were produced in dog trabeculae by replacing 90-95% of the calcium in the bathing solution with strontium. These conditions produced prolonged action potentials accompanied by contractions with two distinct phasic components. The early component disappeared slowly when the remaining Ca ++ was removed, whereas the late component was eliminated quickly when Sr ++ was removed. Manganese ion (0.25 ITIM) preferentially decreased the late component without changing the action potential, whereas caffeine and ryanodine decreased or eliminated the early component. Ryanodine did not alter the action potential. Isoproterenol rapidly increased the early component and, more slowly and to a lesser degree, increased the late component. The results suggest that the early component is caused by intracellular release of activator cation, probably from the sarcoplasmic reticulum, whereas the late component is the result of Sr ++ entry across the sarcolemma, possibly by way of the slow inward current. TWO distinct components of contraction, one fast and one slow, have been shown to exist in mammalian ventricular myocardium under certain conditions. They can be seen in rested state contractions, after a 10-to 15-minute stimulation-free period, in the absense (Allen et al., 1976) or in the presence of an adrenergic agonist (Berescewicz and Reuter, 1977;Seibel et al., 1978), in low-temperature, constant frequency contractions under the influence of noradrenaline (Bogdanov et al., 1979), and after 90% replacement of Ca ++ with Sr ++ (Braveny and Sumbera, 1972). The common characteristic of these conditions is an increase in the duration of the action potential, and, in fact, biphasic contractions can be produced when the plateau of the action potential is lengthened by voltage clamp techniques (Morad and Trautwein, 1968;Braveny and Sumbera, 1970) or by toxins (Coraboeuf et al., 1975;Honerjager and Reiter, 1975). Although it is generally agreed that each component of contraction is due to a specific type of cation release, the site of the cation pools is the subject of some controversy.A number of proposals of the origin of the two cation release sites have been published, one visualizing Ca release from the same site but by different mechanisms (Allen et al., 1976) and the others hypothesizing contractile activation by two morphologically distinct pools (Braveny and Sumbera, 1972; Berescewicz and Reuter, 1977;Seibel et al., 1978;Bogdanov et al., 1979). The present study was designed to try to resolve the question of the origin of biphasic contractions by using specific pharmacological interventions. Strontium-induced resolution of the two components was used because it allows constant, relatively high frequency (0.5 Hz) stimulation while enabling a quantitative comparison of the effects of adrenergic agonists on the separate components to be made. The results are discussed in relation to the other models of two-component contractions. Methods Mechanical ExperimentsMongrel dogs (3-10 kg) of either sex wer...

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“…Caffeine, particularly at high concentrations, has been shown to release Ca2+ from the sarcoplasmic reticulum (Chapman & Leoty, 1976;Endo, 1977) and to inhibit Ca2+ uptake by it (Blinks, Olsen, Jewell & Braveny, 1972;Blayney, Thomas, Muir & Henderson, 1978). To determine whether the amount of Ca2+ associated with the sarcoplasmic reticulum in cells grown with and without T3 is different, the effect of caffeine on the contractile behaviour of cultured myocytes was determined.…”

Section: Sarcoplasmic Reticulumca2+ Contentmentioning

confidence: 99%

Effects of thyroid hormone on calcium handling in cultured chick ventricular cells.

Kim¹,

Smith²

1985

The Journal of Physiology

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SUMMARY1. Mechanisms underlying thyroid hormone-induced changes in myocardial contractile state were investigated by studying the effects of triiodothyronine (T3) on Ca2+ fluxes across the sarcolemmal membrane and Ca2+ handling by the sarcoplasmic reticulum, using spontaneously contracting monolayers of cultured chick embryo ventricular cells.2. Cells were grown in serum-free medium containing either no T3 or 10-8 M-T3 for 48 h. At [Ca2+]. levels of 0-6 and 1-2 mm, the velocity of cell contraction was significantly greater in cells grown in 10-8 M-T3 than in its absence. At higher [Ca2+]0, no differences in the velocity of contraction were noted. 3. 45Ca2+ exchange kinetic studies showed a biexponential pattern with a rapid and a slow component of uptake in cells grown both with and without 10-8 M-T3. The rate of the rapid phase of uptake and total Ca2+ content were higher in cells grown in T3, with the increment in content ascribable to the rapidly exchangeable Ca2+ pool.4. Verapamil partially inhibited the T3-induced increase in the rapidly exchangeable pool. 45Ca2+ uptake in response to a step change to Na+-free medium in the presence of 1 ,/M-verapamil was significantly greater in cells grown in 10-8 M-T3 than in T3-free medium.5. Cells grown in T3 showed 20% greater beating rate than cells grown in its absence. A similar increase in beating rate achieved by lowering [K+]. from 4 0 to 3 0 mM or by electrical stimulation failed to affect the rate of 45Ca2+ uptake or the size of the rapidly exchangeable pool; pacing-induced increases in rate resulted in reduction rather than augmentation of contractile state.6. Ca2+ efflux rate was greater in cells grown in 10-8 M-T3 than in T3-free medium, whereas cells loaded with various levels of Ca2+ acutely by incubation at selected[Ca2+]0 levels had similar efflux rates. Replacement of Na+ by choline in the efflux medium resulted in elevated Ca2+ efflux rates in cells grown both with and without T3; however, it remained greater in cells grown in 10-8 M-T3 than in its absence.7. Caffeine (20 mM) in the efflux medium increased Ca2+ efflux to a greater degree in cells grown in T3 than without it. Caffeine also produced a greater tonic contraction in T3-treated cells than in cells grown in absence of T3 in Na+-and Ca2+-free medium.8. Cellular content of sarcoplasmic reticulum Ca2+-ATPase, as judged by maximal 5-2

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Action of caffeine on calcium transport by isolated fractions of myofibrils, mitochondria, and sarcoplasmic reticulum from rabbit heart.

Cited by 76 publications

References 34 publications

Caffeine reversal of length-dependent changes in myocardial contractile state in the cat.

Caffeine reversal of length-dependent changes in myocardial contractile state in the cat.

Mechanism of biphasic contractions in strontium-treated ventricular muscle.

Effects of thyroid hormone on calcium handling in cultured chick ventricular cells.

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