Rat vs. rabbit ventricle: Ca flux and intracellular Na assessed by ion-selective microelectrodes

Shattock, M. J.; Bers, Donald M.

doi:10.1152/ajpcell.1989.256.4.c813

Cited by 225 publications

(127 citation statements)

References 43 publications

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“…Nevertheless, we were surprised that the large reduction in basal Ca 2+ current in STAA myocytes did not cause a detectable reduction in cellular contraction under basal conditions. Unlike other species, the Ca 2+ store in the sarcoplasmic reticulum in mouse or rat ventricular myocytes is relatively full at rest and at low stimulation frequency (40); therefore, Ca 2+ release and subsequent contraction may be less dependent on Ca 2+ influx as a trigger under basal physiological conditions. In addition, failure to sustain contractions during repetitive stimulation at 1 Hz may reflect the deficiency in Ca 2+ reloading of the sarcoplasmic reticulum due to the large reduction in Ca 2+ influx through STAA Ca V 1.2 channels.…”

Section: Phosphorylation Of Ser1700 and Thr1704 Is Required For Normamentioning

confidence: 97%

Phosphorylation sites required for regulation of cardiac calcium channels in the fight-or-flight response

Westenbroek

Scheuer

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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The undersigned authors wish to note, "The KefFC system of E. coli is maintained in an inactive state by the binding of glutathione (GSH) and is activated by the formation of GSH adducts (GSX), particularly those with bulky substituents. We described two crystal structures with density present in the ligand-binding domain that we interpreted as GSH and GSX. Recently, an independent, experienced crystallographer, who had viewed the structures from our study in a different context, made representations to us that cast doubt on position of the succinimido ring of GSX. We have further reviewed the density maps with the aid of an experienced crystallographer. As a consequence, we believe it is important to draw this altered interpretation of the crystal structures to the attention of readers. In both structures, the density for the backbone of GSH is clear and allows unequivocal assignment of the position of the tripeptide. In PDB coordinate set 3L9X, the density for the succinimido ring is very weak, making interpretation very speculative and the assignment rests on the identity of the ligand added to the crystallization mixture, for which there are two diastereomers in the solutiona possibility that provides some basis for weakening the density. However, in 3L9W there are two anomalies that affect the interpretation of the bound ligand. First, there is no density for the carbon atom attached to the sulfur of GSH and second, there is extra density adjacent to the position of sulfur that could be modelled as a constrained succinimido ring. However, this density could also be water or any other molecule that is trapped in the structure. Thus, while there is good evidence for the peptide, the evidence that it is in the GSH form is uncertain."There are no new data on either the structures or on the gating mechanism. However, we believe that we should be cautious in interpreting the structural data and that the field in general should be made aware of the alternative views of the electron density data. Note that the mutagenesis and spectroscopic data that were presented in the original manuscript are not affected by this alternative interpretation." Tarmo P. The authors note that the following grant should be added to the Acknowledgments: "NIH Grant AG002132." The authors note "The method used for exogenous expression of Ca V 1.2 channels in ref. 32 was incorrectly described as 'viral transduction' in the text. In fact, Yang et al. created transgenic mice with inducible, cardiomyocyte-specific expression of exogenous Ca V 1.2 channels regulated by a tetracycline-inducible promoter. When crossed with a transgenic mouse line expressing doxycycline-regulated reverse transcriptional activator under control of the α-myosin heavy chain protomer, the resulting double transgenic offspring expressed exogenous Ca V 1.2 channels in their cardiac myocytes after treatment with doxycycline. The authors regret the error in describing these methods."www.pnas.org/cgi

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Section: Phosphorylation Of Ser1700 and Thr1704 Is Required For Normamentioning

confidence: 97%

Phosphorylation sites required for regulation of cardiac calcium channels in the fight-or-flight response

Westenbroek

Scheuer

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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“…These authors also employed the microcalorimetric method of measuring the rate of basal heat production of isolated trabeculae, but chose to use trabeculae from the guinea pig instead of from the rat. In this species, as in the rabbit (but in contrast to the rat [148]), the reversal potential of the Na ϩ -Ca 2ϩ exchanger seems to be greatly displaced from the resting membrane potential [88]. As a result, some time is required before [Na ϩ ] i is increased sufficiently to effect a reversal of Na ϩ -Ca 2ϩ exchange.…”

Section: Contributors To the Energymentioning

confidence: 89%

Cardiac Basal Metabolism.

Gibbs

Loiselle²

2001

JJP

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The cardiac basal metabolism is the rate of energy expenditure of the quiescent myocardium. It is also called the resting metabolism or the arrested heart metabolism. It has been measured in numerous ways, and in vivo there is good evidence that it accounts for about 1/5 to 1/3 of the total energy flux. The difficulty arises, however, when the heart is stopped because the magnitude of the basal metabolism depends, as blood viscosity, on how and under what physiological condition it is measured. It is possible for the in vivo basal value to fall to less than 1/5 of its original value without cellular damage or to increase to values 5 times greater than its probable in vivo magnitude (i.e., to rise to values in excess of the energy flux of the normally beating heart) by altering the composition of the perfusion medium. We have written on this subject several times [1][2][3], but believe that developments in knowledge now make it possible for us to speculate in a more informed manner. Since several million openheart operations are performed on arrested hearts worldwide each year, it would seem imperative that we understand the cellular mechanisms that can change the magnitude of basal metabolism.A. V. Hill [4] has pointed out that in examining physiological activities, it is necessary to assume a baseline from which some quantity or rate can be measured. If the energy flux produced by the beating heart were very large compared with the energy flux of the arrested heart, baseline ambiguity would be relatively unimportant. But this is not so in regard to the heart; its basal metabolism is high. Within a species, the basal metabolism of cardiac tissue is several-fold higher than the resting metabolism of skeletal muscle and is an order of magnitude greater than the resting metabolism of amphibian skeletal muscle.Species differences are clearly evident in the magnitude of cardiac basal metabolism, and we believe that the major reason for these differences relates to the leakiness of cell membranes, such as those of the sarcolemma and sarcoplasmic reticulum and those of Japanese Journal of Physiology, 51, 399-426, 2001 Key words: whole hearts, isolated preparations, biochemical contributors, modifiers, species difference, temperature, substrate, hypoxia. Abstract:We endeavor to show that the metabolism of the nonbeating heart can vary over an extreme range: from values approximating those measured in the beating heart to values of only a small fraction of normal-perhaps mimicking the situation of nonflow arrest during cardiac bypass surgery. We discuss some of the technical issues that make it difficult to establish the magnitude of basal metabolism in vivo. We consider some of the likely contributors to its magnitude and point out that the biochemical reasons for a sizable fraction of the heart's basal ATP usage remain unresolved. We consider many of the physiological factors that can alter the basal metabolic rate, stressing the importance of substrate supply. We point out that the protective effect of hypothermia ...

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“…Developed tension and peak systolic [Ca 2+ ] ( fall with increased frequency (in the frequency range we examined) in rat cardiac tissue, 33 which distinguishes it from other species. 34 - 35 This may be due to the observation that calcium efflux is predominant during systole via the Na + -Ca 2+ exchanger, whereas in other species calcium influx is greater than efflux during systole. 35 The reverse is true during diastole, during which calcium influx predominates in rat cardiac tissue.…”

Section: Discussionmentioning

confidence: 99%

Calcium dependency of frequency-stimulated atrial natriuretic peptide secretion.

Schiebinger

Cragoe

1994

Hypertension

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In this study we examined the mechanism whereby atrial natriuretic peptide secretion is increased when the frequency of contraction is raised from 2 to 5 Hz. We tested the hypothesis that calcium plays a significant role in the frequency-stimulated response. Using superfused rat left atria, we found that lowering the superfusate calcium concentration from 1.8 to 0.2 mmol/L abolished the frequency-stimulated atrial natriuretic peptide secretory response. Superfusion with ryanodine (1 /xmol/L), an inhibitor of sarcoplasmic reticulum calcium release, resulted in a minimal inhibitory effect. Superfusion with 50 junol/L nitrendipine or 10 junol/L diltiazem inhibited the frequency-stimulated response by 46% to 48%. The lack of total inhibition suggested that an additional mechanism of calcium influx was involved, namely, inward calcium movement carried by Na + -Ca 2+ exchange. As intracellular sodium has been reported to rise with an increase in beat frequency, a fall in the sodium gradient would favor inward calcium movement by Na + -Ca 2+ exchange. Because we could not directly assess the role of Na + -Ca 2+ exchange in this experimental paradigm, we examined the effect of lowering the transmembrane sodium gradient on atrial natriuretic peptide secretion by superfusion with the sodium channel activator A trial tachycardias are associated with a rise in / \ plasma atrial natriuretic peptide (ANP) lev-A.JL els. 15 Using an isolated superfused rat atrial preparation, we have found that increasing the frequency of atrial contraction directly increases ANP secretion 6 ; this observation has been confirmed. 7 In the present study, we examined the mechanisms whereby an increase in the frequency of contraction enhances ANP secretion.It has been reported that raising the contraction frequency increases intracellular sodium activity (a' N> ) in rat atrial muscle. 8 In cardiac tissue, a rise in a' N , results in an increase in cytosolic calcium via Na + -Ca 2+exchange. 910 We therefore tested the hypothesis that calcium plays a significant role in the frequency-stimulated ANP secretory response because we and others have noted that calcium appears to play an important role in stimulated ANP secretion. 1115In addition, we attempted to determine the source of the rise in a' Nt , speculating that an increase in Na + -H + antiporter activity may contribute.

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Rat vs. rabbit ventricle: Ca flux and intracellular Na assessed by ion-selective microelectrodes

Cited by 225 publications

References 43 publications

Phosphorylation sites required for regulation of cardiac calcium channels in the fight-or-flight response

Phosphorylation sites required for regulation of cardiac calcium channels in the fight-or-flight response

Cardiac Basal Metabolism.

Calcium dependency of frequency-stimulated atrial natriuretic peptide secretion.

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