MECHANISM OF CALCIUM–INDUCED RELEASE OF CALCIUM FROM THE SARCOPLASMIC RETICULUM OF SKINNED CARDIAC CELLS STUDIED WITH POTENTIAL–SENSITIVE DYES

1981 ◽  
pp. 237-255 ◽  
Author(s):  
Alexandre Fabiato
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Cardiac Cells

scholarly journals L-type Ca2+ channels in the heart: Structure and regulation

Medicina ◽  
2008 ◽  
Vol 44 (7) ◽  
pp. 491 ◽  
Author(s):  
Rimantas Treinys ◽  
Jonas Jurevičius
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Cardiac Myocytes ◽  
Extracellular Space ◽  
Heart Diseases ◽  
Life Quality ◽  
Cardiac Cells ◽  
Cell Cytoplasm ◽  
Regulation Mechanisms ◽  
Important System ◽  
Ca2 Channels

This review analyzes the structure and regulation mechanisms of voltagedependent L-type Ca2+ channel in the heart. L-type Ca2+ channels in the heart are composed of four different polypeptide subunits, and the pore-forming subunit a1 is the most important part of the channel. In cardiac myocytes, Ca2+ enter cell cytoplasm from extracellular space mainly through L-type Ca2+ channels; these channels are very important system in heart Ca2+ uptake regulation. L-type Ca2+ channels are responsible for the activation of sarcoplasmic reticulum Ca2+ channels (RyR2) and force of muscle contraction generation in heart; hence, activity of the heart depends on L-type Ca2+ channels. Phosphorylation of channel-forming subunits by different kinases is one of the most important ways to change the activity of L-type Ca2+ channel. Additionally, the activity of L-type Ca2+ channels depends on Ca2+ concentration in cytoplasm. Ca2+ current in cardiac cells can facilitate, and this process is regulated by phosphorylation of L-type Ca2+ channels and intracellular Ca2+ concentration. Disturbances in cellular Ca2+ transport and regulation of L-type Ca2+ channels are directly related to heart diseases, life quality, and life span.

Pacemaker activity in the insect (T. molitor) heart: role of the sarcoplasmic reticulum

2011 ◽  
Vol 301 (6) ◽  
pp. R1838-R1845 ◽  
Author(s):  
Danielle F. Feliciano ◽  
Rosana A. Bassani ◽  
Pedro X. Oliveira ◽  
José W. M. Bassani
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Cardiac Cells ◽  
Pacemaker Activity ◽  
Electrophysiological Properties ◽  
Chronotropic Response ◽  
Different Types ◽  
Mealworm Beetle ◽  
Beating Rate

The electrophysiological properties of the myogenic cardiac cells of insects have been analyzed, but the mechanisms that regulate the pacemaker activity have not been elucidated yet. In mammalian pacemaker cells, different types of membrane ion channels seem to be sequentially activated, perhaps in a cooperative fashion with the current generated by Ca2+ extrusion mediated by the electrogenic Na+/Ca2+ exchanger, which is sustained by the diastolic sarcoplasmic reticulum (SR) Ca2+ release. The objective of the present work was to investigate the role of the SR function on the basal beating rate (BR), and BR modulation by extracellular Ca2+ concentration ([Ca2+]o) and neurotransmitters in the in situ dorsal vessel (heart) of the mealworm beetle Tenebrio molitor . The main observations were as follows: 1) basal BR was reduced by 50% by inhibition of SR function, but not affected by perfusion with CsCl or ZD7288; 2) spontaneous activity was abolished by Cd2+; 3) a robust positive chronotropic response could be elicited to serotonin (5-HT), but not to norepinephrine or carbamylcholine; 4) SR inhibition abolished the sustained chronotropic stimulation by [Ca2+]o elevation and by 5-HT, while the latter was unaffected by CsCl. It is concluded that, in T. molitor heart, BR is markedly, but not exclusively, dependent on the SR function, and that BR control and modulation by both [Ca2+]o and 5-HT requires a functional SR.

Junctional Sarcoplasmic Reticulum in Excitation-Contraction-Coupling

1982 ◽  
Vol 40 ◽  
pp. 136-137
Author(s):  
J.R. Sommer ◽  
E. Bossen ◽  
A. Fabiato
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Action Potential ◽  
Muscle Contraction ◽  
Cardiac Cells ◽  
Close Apposition ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Terminal Cisterna ◽  
Voltage Dependent ◽  
Junctional Sarcoplasmic Reticulum

The junctional sarcoplasmic reticulum (JSR, syn. terminal cisterna) is implicated in Ca++storage and release for muscle contraction. Its discrete ultrastructure permits distinction from the rest of the SR (free SR) even when it occurs without plasmalemmal contact, e.g. as extended JSR (EJSR) in bird, and corbular SR (CSR) in mammalian cardiac cells. The close apposition of JSR to plasmalemma via junctional processes is central to proposed mechanisms of translating voltage-dependent charge transfers at the plasmalemma during the action potential into Ca++release from the JSR. These hypotheses are put into question by the existence of EJSR (and CSR) which in birds constitutes 70-80% of the total JSR. An alternate hypothesis proposes, at least for cardiac cells, that Ca++entering the cell during excitation causes additional Ca++to be freed intracellularly. The notion of a chemical transmitter acting by diffusion is attractive because it will allow for the anomalous topography of EJSR, especially since bird cardiac cells have only about half the diameter of their mammalian relatives and have no transverse tubules.

Two physiological agents that appear to facilitate calcium discharge from the sarcoplasmic reticulum in frog heart cells: adrenalin and ATP

1981 ◽  
Vol 213 (1192) ◽  
pp. 325-344 ◽  
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Preceding Paper ◽  
Cardiac Cells ◽  
Frog Heart ◽  
Heart Cells ◽  
Physiological Importance ◽  
Low Concentrations ◽  
Circulatory Control ◽  
Sarcoplasmic Reticulum Calcium ◽  
Ventricular Trabeculae

The α-adrenergic effect of adrenalin and the action of ATP and other nucleotides have been examined in single trabeculae of frog heart by means of procedures developed in the preceding paper (Niedergerke & Page 1981). The results suggest that both adrenalin and ATP are able, in conjunction with the action potential, to facilitate the discharge of calcium from the sarcoplasmic reticulum in at least some of the cardiac cells. As a result, the strength of the twitch is enhanced. As shown previously for the action of caffeine, this calcium discharge was not maintained, declining rapidly, together with the twitch tension, as the sarcoplasmic reticulum calcium store became depleted. Trabeculae from atrium and ventricle differed in their propensity to respond to these two substances. Thus, α- adrenergic responses were obtained in some 30% of the atrial, but in none of the ventricular, trabeculae examined. On the other hand, both kinds of trabecula gave ATP responses, but these tended to be weaker and required higher concentrations in ventricle than atrium. The possibility that the two responses are of physiological importance is suggested by the low concentrations (≼ 5 x 10 -7 M) needed to produce large tension increases. A tentative hypothesis is advanced according to which α-catecholamine and ATP effects participate in circulatory control by initiating a rapid boost of cardiac pump activity, preparatory to the slower but better maintained β-catecholamine action.

Calcium-induced release of calcium from the cardiac sarcoplasmic reticulum

1983 ◽  
Vol 245 (1) ◽  
pp. C1-C14 ◽  
Author(s):  
A. Fabiato
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Negative Feedback ◽  
Slow Component ◽  
Alternative Hypothesis ◽  
Cardiac Cells ◽  
Cardiac Cell ◽  
Cardiac Sarcoplasmic Reticulum ◽  
Ventricular Cell ◽  
Small Change ◽  
Ca2 Channels

The hypothesis of a Ca2+-induced Ca2+ release (CICR) from the sarcoplasmic reticulum (SR) is supported by experiments done in skinned cardiac cells (sarcolemma removed by microdissection). According to this hypothesis, the transsarcolemmal Ca2+ influx does not activate the myofilaments directly but through the induction of a Ca2+ release from the SR. The stimulus gating CICR is not a small change in free Ca2+ concentration (delta[free Ca2+]) outside the SR but a function of the rate of this change (delta[free Ca2+/delta t]). The initial relatively fast component of the transsarcolemmal Ca2+ current would trigger Ca2+ release; the subsequent slow component, perhaps corresponding to noninactivating Ca2+ channels, would load the SR with an amount of Ca2+ available for release during subsequent beats. Inactivation of CICR is caused by the large increase of [free Ca2+] outside the SR resulting from Ca2+ release, which inhibits further release. This negative feedback helps to explain that CICR is not all or none. During relaxation the Ca2+ reaccumulation in the SR is backed up by the Ca2+ efflux across the sarcolemma through Na+-Ca2+ exchange and the sarcolemmal Ca2+ pump. Computations of the Ca2+ buffering in the mammalian ventricular cell and of the systolic transsarcolemmal Ca2+ influx do not support the alternative hypothesis that this influx of Ca2+ is large enough to activate the myofilaments directly. Yet the hypothesis of a CICR can be challenged because of many problems and uncertainties related to the preparations and methods used for skinned cardiac cell experiments.

Regulation of calcium transport in cardiac cells

1984 ◽  
Vol 62 (1) ◽  
pp. 9-22 ◽  
Author(s):  
Adil E. Shamoo ◽  
Indu S. Ambudkar
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Calcium Channel ◽  
Calcium Homeostasis ◽  
Calcium Transport ◽  
Cardiac Cells ◽  
Transport Systems ◽  
Sodium Calcium Exchanger ◽  
Inotropic Effects ◽  
Cellular Calcium ◽  
Sodium Calcium

Calcium transporting systems and the regulatory events accompanying them are pivotal in the function of the cardiac cell. The concerted involvement of the various membranes achieve cellular calcium homeostasis that can also respond to the physiological exigencies of the cell. Three membrane systems are primarily involved; the sarcolemma, sarcoplasmic reticulum, and the mitochondria. The various Ca2+ transport systems that have been described in these membranes are as follows: the calcium channel, Ca2+-ATPase, Ca2+–Mg2+ ATPase, and sodium–calcium exchanger in the sarcolemma; the Ca2+–Mg2+ ATPase and a possible calcium channel in the sarcoplasmic reticulum; and the sodium–calcium exchanger and electrophoretic calcium uniporter in the mitochondrial inner membrane. These systems mediate calcium fluxes to maintain physiological cytosolic calcium concentrations. β-Adrenergic hormones regulate calcium transport systems in sarcolemma and sarcoplasmic reticulum, while α-adrenergic hormones modulate those in the mitochondria and probably in the sarcolemma. The response to these hormones is initiated at the sarcolemma, which contains the specific receptors. Intracellularly the effects are propagated by secondary messengers, e.g., cAMP, calcium, and lipid changes. Specific proteins are also involved in these events. Phospholamban, a 22 000 dalton protein, is involved in mediating the cAMP-dependent inotropic effects, by activating the Ca2+–Mg2+ ATPase of the sarcoplasmic reticulum. Alterations in any one of the systems involved in the regulation of calcium transport or in the calcium transport systems per se, would then result in drastic alterations in the cellular calcium homeostasis. Such effects could be of significance in cellular dysfunction during cardiac disease.

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