The effect of ryanodine on the contraction of isolated frog atrial trabeculae is triggered by caffeine

Tunstall, J.; Ra, Chisei

doi:10.1113/expphysiol.1994.sp003778

Cited by 6 publications

(6 citation statements)

References 22 publications

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“…As in both skeletal muscle and rat ventricle fibres the SR provides a cellular store for calcium that is responsible for the activation of contraction, it is reasonable that, assuming the SR in the frog heart to have the same function, a much smaller capacity for this purpose exists in these heart cells. However, even though most, if not all, of the Ca 2+ required for the activation of the twitch tension in frog heart cells is supplied by the inward Ca 2+ current through the surface membrane (Niedergerke et al 1976, Tunstall & Chapman 1994, atrial and ventricular cells may rely on Ca 2+ release from the SR under special conditions, such as adrenergic and/or P2 purinergic stimulation (Niedergerke & Page 1981).…”

Section: Sarcoplasmic Reticulummentioning

confidence: 99%

Phospholamban and cardiac function: a comparative perspective in vertebrates

Cerra¹,

Imbrogno

2012

Acta Physiol

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Phospholamban (PLN) is a small phosphoprotein closely associated with the cardiac sarcoplasmic reticulum (SR). Dephosphorylated PLN tonically inhibits the SR Ca-ATPase (SERCA2a), while phosphorylation at Ser16 by PKA and Thr17 by Ca 2+ /calmodulin-dependent protein kinase (CaMKII) relieves the inhibition, and this increases SR Ca 2+ uptake. For this reason, PLN is one of the major determinants of cardiac contractility and relaxation. In this review, we attempted to highlight the functional significance of PLN in vertebrate cardiac physiology. We will refer to the huge literature on mammals in order to describe the molecular characteristics of this protein, its interaction with SERCA2a and its role in the regulation of the mechanic and the electric performance of the heart under basal conditions, in the presence of chemical and physical stresses, such as b-adrenergic stimulation, response to stretch, force-frequency relationship and intracellular acidosis. Our aim is to provide the basis to discuss the role of PLN also on the cardiac function of nonmammalian vertebrates, because so far this aspect has been almost neglected. Accordingly, when possible, the literature on PLN will be analysed taking into account the nonuniform cardiac structural and functional characteristics encountered in ectothermic vertebrates, such as the peculiar and variable organization of the SR, the large spectrum of response to stresses and the disaptive absence of crucial proteins (i.e. haemoglobinless and myoglobinless species). Intracellular [Ca 2+ ] oscillation, a major determinant of the myocardial contraction/relaxation cycle, is governed by a number of transporters. They include sarcolemmal L-type Ca 2+ channels, Na + /Ca 2+ exchanger, the plasma membrane Ca 2+ pump, several sarcoplasmic reticulum (SR) membrane proteins such as the ryanodine receptors, as well as the complex formed by the sarcoplasmic membrane Ca 2+ pump (SERCA2a) and its associated regulatory protein phospholamban (PLN). The name of this protein, which means 'phosphate receptor' (from phosphate and the Greek word kalbamx = I receive), very appropriately reflects its function. After its discovery by Katz and co-workers in cardiac mammalian microsomes [for complete references, see Katz (2006)], many works have largely demonstrated that, during a normal cardiac cycle, alternate PLN phosphorylation/dephosphorylation determines SERCA2a on/off state, and thus the rate of SR refilling with Ca 2+ , with a consequent strong impact on myocardial relaxation and contraction. At the level of sinoatrial node cells, the SERCA2a-PLN system functions as an intracellular 'Ca 2+ ' clock,

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Section: Sarcoplasmic Reticulummentioning

confidence: 99%

Phospholamban and cardiac function: a comparative perspective in vertebrates

Cerra¹,

Imbrogno

2012

Acta Physiol

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“…In the ventricle of rat heart, the SR is quite abundant and block of the SR Ca 21 pump by thapsigargin, resulting in depletion of the SR Ca 21 stores, reduces twitch tension and Ca 21 transients by 80% (Inesi et al, 1998). At the other end of the spectrum, frog myocardium relies on extracellular Ca 21 , SR Ca 21 release is of small magnitude and its role in e-c coupling has been debated (Kavaler, 1974;Anderson et al, 1977;Niedergerke et al, 1976;Niedergerke and Page, 1981a,b;Morad and Cleemann, 1987;Tunstall and Chapman, 1994). Indeed, it is thought that SR Ca 21 in frog myocardium is called into play only under conditions of adrenergic and/or P 2 purinergic stimulation (Niedergerke and Page, 1981b).…”

Section: Introductionmentioning

confidence: 99%

“…In ventricle, on the other hand, the effect of caffeine is either absent (Niedergerke and Page, 1981a) or very small (Chapman and Miller, 1974), and the latter may be attributable to a direct effect on the myofibrils at the high concentrations of caffeine used (S. Page, personal communication; see also Wendt and Stephenson, 1983). In frog atrium ryanodine leads to a transient increase in twitch tension if applied in the presence of caffeine, but seems to have no effect in its absence (Tunstall and Chapman, 1994). No effect of ryanodine was reported for the ventricle, even though a large range of concentrations was used (Ciofalo, 1973).…”

Section: Introductionmentioning

confidence: 99%

Location of Ryanodine and Dihydropyridine Receptors in Frog Myocardium

Tijskens

Meissner

Franzini‐Armstrong

2003

Biophysical Journal

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Frog myocardium depends almost entirely on calcium entry from extracellular spaces for its beat-to-beat activation. Atrial myocardium additionally shows internal calcium release under certain conditions, but internal release in the ventricle is absent or very low. We have examined the content and distribution of the sarcoplasmic reticulum (SR) calcium release channels (ryanodine receptors, RyRs) and the surface membrane calcium channels (dihydropyridine receptors, DHPRs) in myocardium from the two atria and the ventricle of the frog heart using binding of radioactive ryanodine, immunolabeling of RyR and DHPR, and thin section and freeze-fracture electron microscopy. In cells from both types of chambers, the SR forms peripheral couplings and in both chambers peripheral couplings colocalize with clusters of DHPRs. However, although a low level of high affinity binding of ryanodine is detectable and RyRs are present in peripheral couplings of the atrium, the ventricle shows essentially no ryanodine binding and RyRs are not detectable either by electron microscopy or immunolabeling. The results are consistent with the lack of internal calcium release in the ventricle, and raise questions regarding the significance of DHPR at peripheral couplings in the absence of RyR. Interestingly, the free SR membrane in both heart chambers shows a low but equal density of intramembrane particles representing the Ca(2+) ATPase.

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“…Consistent with this finding, voltage‐clamp studies of frog ventricle showed that the Ca 2+ involved in the activation of tension arose primarily from the extracellular space 26 . Subsequently, studies in frog atrial cells using ryanodine and caffeine suggested that some Ca 2+ was stored in and capable of being released from the SR 27 . Nevertheless, the prevalent view remains that, in amphibian heart tissue, the SR is not a major source of Ca 2+ during the normal contraction 22 …”

Section: Is Sr In the Amphibian Pacemaker Cell Capable Of Releasing Cmentioning

confidence: 89%

Proceedings of the Australian Physiological and Pharmacological Society Symposium: New Frontiers in Muscle Research Does Ca²⁺ release from the sarcoplasmic reticulum influence heart rate?

Allen

2001

Clin Exp Pharma Physio

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1. The present review summarizes the evidence that Ca2+ release from the sarcoplasmic reticulum (SR) is an important contributor to the systolic rise in [Ca2+]i (the Ca2+ transient) and influences the pacemaker firing rate. 2. We believe that the mechanism whereby [Ca2+]i influences firing rate is through the dependence of the Na+-Ca2+ exchanger on [Ca2+]i. 3. Extrusion of Ca2+ by the electrogenic Na+-Ca2+ exchanger produces an inward current that contributes to the pacemaker currents. Confocal images of Ca2+ indicate the distribution of [Ca2+]i and Ca2+ sparks add to the evidence that Ca2+ release from SR is involved in pacemaker activity. 4. The normal pathway for increased heart rate is sympathetic activation; we discuss the evidence that part of the chronotropic effect of beta-adrenoceptor stimulation is through the modulation of SR Ca2+ release. 5. These studies show that Ca2+ handling by the pacemaker cells makes an important contribution to the regulation of pacemaker activity.

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The effect of ryanodine on the contraction of isolated frog atrial trabeculae is triggered by caffeine

Cited by 6 publications

References 22 publications

Phospholamban and cardiac function: a comparative perspective in vertebrates

Phospholamban and cardiac function: a comparative perspective in vertebrates

Location of Ryanodine and Dihydropyridine Receptors in Frog Myocardium

Proceedings of the Australian Physiological and Pharmacological Society Symposium: New Frontiers in Muscle Research Does Ca²⁺ release from the sarcoplasmic reticulum influence heart rate?

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The effect of ryanodine on the contraction of isolated frog atrial trabeculae is triggered by caffeine

Cited by 6 publications

References 22 publications

Phospholamban and cardiac function: a comparative perspective in vertebrates

Phospholamban and cardiac function: a comparative perspective in vertebrates

Location of Ryanodine and Dihydropyridine Receptors in Frog Myocardium

Proceedings of the Australian Physiological and Pharmacological Society Symposium: New Frontiers in Muscle Research Does Ca2+ release from the sarcoplasmic reticulum influence heart rate?

Contact Info

Product

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Proceedings of the Australian Physiological and Pharmacological Society Symposium: New Frontiers in Muscle Research Does Ca²⁺ release from the sarcoplasmic reticulum influence heart rate?