scholarly journals Spontaneous myogenic fasciculation associated with the lengthening of cardiac muscle in response to static preloading

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Shouyan Fan ◽  
Lingfeng Gao ◽  
Annie Christel Bell ◽  
Joseph Akparibila Azure ◽  
Yang Wang
Keyword(s):  
Cardiac Muscle ◽  
Striated Muscles ◽  
Force Enhancement ◽  
Static Stretch ◽  
Relaxation Period ◽  
Time Integral ◽  
Intracellular Ca ◽  
Tension Time ◽  
Cardiac Relaxation

AbstractForce enhancement is one kind of myogenic spontaneous fasciculation in lengthening preload striated muscles. In cardiac muscle, the role of this biomechanical event is not well established. The physiological passive property is an essential part for maintaining normal diastole in the heart. In excessive preload heart, force enhancement relative erratic passive properties may cause muscle decompensating, implicate in the development of diastolic dysfunction. In this study, the force enhancement occurrence in mouse cardiac papillary muscle was evaluated by a microstepping stretch method. The intracellular Ca2+ redistribution during occurrence of force enhancement was monitored in real-time by a Flou-3 (2 mM) indicator. The force enhancement amplitude, the enhancement of the prolongation time, and the tension–time integral were analyzed by myography. The results indicated that the force enhancement occurred immediately after active stretching and was rapidly enhanced during sustained static stretch. The presence of the force and the increase in the amplitude synchronized with the acquisition and immediate transfer of Ca2+ to adjacent fibres. In highly preloaded fibres, the enhancement exceeded the maximum passive tension (from 4.49 ± 0.43 N/mm2 to 6.20 ± 0.51 N/mm2). The occurrence of force enhancement were unstable in each static stretch. The increased enhancement amplitude combined with the reduced prolongation time to induce a reduction in the tension–time integral. We concluded that intracellular Ca2+-synchronized force enhancement is one kind of interruption event in excessive preload cardiac muscle. During the cardiac muscle in its passive relaxation period, the occurrence of this interruption affected the rhythmic stability of the cardiac relaxation cycle.

scholarly journals The static preload associated myogenic spontaneous fasciculation response in lengthening cardiac muscle

2021 ◽  
Author(s):  
Shouyan Fan ◽  
Lingfeng Gao ◽  
Annie Christel Bell ◽  
Joseph Akparibila Azure ◽  
Yang Wang
Keyword(s):  
Cardiac Muscle ◽  
Passive Tension ◽  
Force Enhancement ◽  
Static Stretch ◽  
Time Integral ◽  
Physiological Properties ◽  
Intracellular Ca ◽  
Tension Time ◽  
Cardiac Relaxation ◽  
Contraction Cycle

Abstract The passive tension force enhancement is one kind of myogenic spontaneous fasciculation in muscles. However, its physiological properties in cardiac fibres are not well known. In this study, mice cardiac papillary muscle spontaneous force enhancement was evaluated by micro stepping stretch method. The occurrence of spontaneous force and real time cardiac fibre Ca2+ redistribution was tranced by Flou-3 (2mM) indicator. Force enhancement amplitude, enhancement prolonging time, and tension–time integral were analysis by myograph analyser. The results indicated that the spontaneous force occurred immediately after the active stretch, rapidly enhanced during tolerating the sustained static stretch. The force occurrence and amplitude enhance synchronized with the Ca2+ recruitment and lightning transmitted to adjacent fibres. In high preload fibres, the enhancement was forceful to over its maximum passive tension (6.20 ± 0.51 N/mm2 to 4.49 ± 0.43 N/mm2). The force occurrences were unsteadiness in each stretch. The increased enhancement amplitude combining with the shortening prolonging time induced reduction of tension–time integral. We concluded that the intracellular Ca2+ synchronized force enhancement is one kind of interruption event in overloading cardiac fibres. This interruption occurred during the relaxation processing in cardiac muscle, therefore affect the rhythmic stability of cardiac relaxation-contraction cycle.

Adenosine as a mediator of postcontraction hyperemia in dog gracilis muscle

1984 ◽  
Vol 246 (2) ◽  
pp. H274-H282 ◽  
Author(s):  
J. M. Kille ◽  
R. E. Klabunde
Keyword(s):  
Linear Regression ◽  
Muscular Contraction ◽  
Saline Control ◽  
Excess Oxygen ◽  
Regression Analyses ◽  
Time Integral ◽  
Transport Inhibitor ◽  
Tension Time ◽  
Adenosine Transport

The role of adenosine in postcontraction hyperemia (PCH) following sustained, maximal isometric contractions was studied in free-flowing dog gracilis muscles. The hemodynamic responses to contraction were examined in the presence and absence of dipyridamole (an adenosine transport inhibitor), erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA, an adenosine deaminase inhibitor), or alpha, beta-methyleneadenosine-5'-diphosphate (AOPCP, an inhibitor of 5'-nucleotidase). Each muscle was stimulated to contract for 1, 3, 5, and 10 s during saline and drug infusions. For each contraction, the tension-time integral (TT), excess flow (EQ), and excess oxygen consumption (EVo2) were computed. Linear regression analyses were then performed on EQ vs. TT, EVo2 vs. TT, and EQ vs. EVo2. An alteration of the PCH response by the drug was determined as any significant change from the saline control in the slope of the linear regression of EQ vs. EVo2. Dipyridamole and EHNA caused increases of 73 and 48%, respectively, in the slope of EQ vs. EVo2, whereas AOPCP decreased the slope by 41%. The changes in the PCH produced by these drugs are consistent with the hypothesis that an increase in interstitial adenosine during muscular contraction contributes to PCH.

scholarly journals From syncitium to regulated pump: a cardiac muscle cellular update

2011 ◽  
Vol 35 (1) ◽  
pp. 22-27 ◽  
Author(s):  
Donna H. Korzick
Keyword(s):  
Cardiac Muscle ◽  
Intracellular Signaling ◽  
Ventricular Myocytes ◽  
Cellular Events ◽  
Intracellular Ca ◽  
Health And Disease ◽  
Cardiac Excitation ◽  
And Function ◽  
Cardiac Automaticity

The primary purpose of this article is to present a basic overview of some key teaching concepts that should be considered for inclusion in an six- to eight-lecture introductory block on the regulation of cardiac performance for graduate students. Within the context of cardiac excitation-contraction coupling, this review incorporates information on Ca2+ microdomains and local control theory, with particular emphasis on the role of Ca2+ sparks as a key regulatory component of ventricular myocyte contraction dynamics. Recent information pertaining to local Ca2+ cycling in sinoatrial nodal cells (SANCs) as a mechanism underlying cardiac automaticity is also presented as part of the recently described coupled-clock pacemaker system. The details of this regulation are emerging; however, the notion that the sequestration and release of Ca2+ from internal stores in SANCs (similar to that observed in ventricular myocytes) regulates the rhythmic excitation of the heart (i.e., membrane ion channels) is an important advancement in this area. The regulatory role of cardiac adrenergic receptors on cardiac rate and function is also included, and fundamental concepts related to intracellular signaling are discussed. An important point of emphasis is that whole organ cardiac dynamics can be traced back to cellular events regulating intracellular Ca2+ homeostasis and, as such, provides an important conceptual framework from which students can begin to think about whole organ physiology in health and disease. Greater synchrony of Ca2+-regulatory mechanisms between ventricular and pacemaker cells should enhance student comprehension of complex regulatory phenomenon in cardiac muscle.

Role of extracellular calcium on heart muscle energetics: effects of verapamil

1990 ◽  
Vol 258 (1) ◽  
pp. H64-H72 ◽  
Author(s):  
J. E. Ponce-Hornos ◽  
E. A. Musi ◽  
P. Bonazzola
Keyword(s):  
Heat Production ◽  
Fiber Length ◽  
Muscle Length ◽  
Muscle Energetics ◽  
Inotropic Effects ◽  
Time Integral ◽  
Myocardial Contractile Force ◽  
Tension Time ◽  
Myocardial Contractile

The mechanical and energetic effects of verapamil (VER) and reduction of extracellular Ca concentration ([Ca]o) were studied in the interventricular rabbit septa and the dog papillary muscle. Even though the negative inotropic effects of VER [i.e., decrease in developed tension (T), maximal rates of contraction (+T) and relaxation (-T), and tension time integral] qualitatively resemble [Ca]o reduction, VER also elicited an anti-relaxant effect (decrease in -T/T and prolongation of the last phase of relaxation) that was not found with [Ca]o reduction. Resting heat production was similar in both preparations and remained unaffected either by changes in [Ca]o or by the presence of VER. The ratio between T and active heat production per beat (H'a) under constant fiber length decreased with VER, and this decreased economy of contraction was more marked with the increase in contraction frequency. Conversely, the T/H'a remained unaltered with changes in [Ca]o. Tension-independent heat decreased in the presence of VER and, although muscle economy can be improved by increasing muscle length in a VER-treated muscle, it is not possible to achieve either the maximal T or the maximal contraction economy that can be obtained by stretching a nontreated muscle. It may be concluded that at constant fiber length and frequency of contraction VER decreases myocardial contractile force, impairs relaxation, and decreases contraction economy. Neither the mechanical nor the energetic effects of VER can be explained solely on the basis of a reduced extracellular Ca availability, so that either the density of the Ca that enters through the channel is different from that of other sources of Ca or VER has an effect on the cross-bridge cycling mechanism.

scholarly journals TRIC-A Channel Maintains Store Calcium Handling by Interacting With Type 2 Ryanodine Receptor in Cardiac Muscle

2020 ◽  
Vol 126 (4) ◽  
pp. 417-435 ◽  
Author(s):  
Xinyu Zhou ◽  
Ki Ho Park ◽  
Daiju Yamazaki ◽  
Pei-hui Lin ◽  
Miyuki Nishi ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Sarcoplasmic Reticulum ◽  
Cardiac Muscle ◽  
Ryanodine Receptor ◽  
Calcium Handling ◽  
Striated Muscles ◽  
Human Embryonic Kidney Cells ◽  
Intracellular Ca ◽  
Ion Conducting

Rationale: Trimeric intracellular cation (TRIC)-A and B are distributed to endoplasmic reticulum/sarcoplasmic reticulum intracellular Ca 2+ stores. The crystal structure of TRIC has been determined, confirming the homotrimeric structure of a potassium channel. While the pore architectures of TRIC-A and TRIC-B are conserved, the carboxyl-terminal tail (CTT) domains of TRIC-A and TRIC-B are different from each other. Aside from its recognized role as a counterion channel that participates in excitation-contraction coupling of striated muscles, the physiological function of TRIC-A in heart physiology and disease has remained largely unexplored. Objective: In cardiomyocytes, spontaneous Ca 2+ waves, triggered by store overload–induced Ca 2+ release mediated by the RyR 2 (type 2 ryanodine receptor), develop extrasystolic contractions often associated with arrhythmic events. Here, we test the hypothesis that TRIC-A is a physiological component of RyR 2 -mediated Ca 2+ release machinery that directly modulates store overload–induced Ca 2+ release activity via CTT. Methods and Results: We show that cardiomyocytes derived from the TRIC-A −/− (TRIC-A knockout) mice display dysregulated Ca 2+ movement across sarcoplasmic reticulum. Biochemical studies demonstrate a direct interaction between CTT-A and RyR 2 . Modeling and docking studies reveal potential sites on RyR 2 that show differential interactions with CTT-A and CTT-B. In HEK293 (human embryonic kidney) cells with stable expression of RyR 2 , transient expression of TRIC-A, but not TRIC-B, leads to apparent suppression of spontaneous Ca 2+ oscillations. Ca 2+ measurements using the cytosolic indicator Fura-2 and the endoplasmic reticulum luminal store indicator D1ER suggest that TRIC-A enhances Ca 2+ leak across the endoplasmic reticulum by directly targeting RyR 2 to modulate store overload–induced Ca 2+ release. Moreover, synthetic CTT-A peptide facilitates RyR 2 activity in lipid bilayer reconstitution system, enhances Ca 2+ sparks in permeabilized TRIC-A −/− cardiomyocytes, and induces intracellular Ca 2+ release after microinjection into isolated cardiomyocytes, whereas such effects were not observed with the CTT-B peptide. In response to isoproterenol stimulation, the TRIC-A −/− mice display irregular ECG and develop more fibrosis than the WT (wild type) littermates. Conclusions: In addition to the ion-conducting function, TRIC-A functions as an accessory protein of RyR 2 to modulate sarcoplasmic reticulum Ca 2+ handling in cardiac muscle.

scholarly journals The role of calcium homeostasis remodeling in inherited cardiac arrhythmia syndromes

2021 ◽  
Author(s):  
Shanna Hamilton ◽  
Roland Veress ◽  
Andriy Belevych ◽  
Dmitry Terentyev
Keyword(s):  
Cardiac Arrhythmia ◽  
Cardiac Death ◽  
Ventricular Arrhythmias ◽  
Polymorphic Ventricular Tachycardia ◽  
Genetic Mutations ◽  
Strong Basis ◽  
Functional Changes ◽  
Intracellular Ca ◽  
Qt Syndrome

AbstractSudden cardiac death due to malignant ventricular arrhythmias remains the major cause of mortality in the postindustrial world. Defective intracellular Ca2+ homeostasis has been well established as a key contributing factor to the enhanced propensity for arrhythmia in acquired cardiac disease, such as heart failure or diabetic cardiomyopathy. More recent advances provide a strong basis to the emerging view that hereditary cardiac arrhythmia syndromes are accompanied by maladaptive remodeling of Ca2+ homeostasis which substantially increases arrhythmic risk. This brief review will focus on functional changes in elements of Ca2+ handling machinery in cardiomyocytes that occur secondary to genetic mutations associated with catecholaminergic polymorphic ventricular tachycardia, and long QT syndrome.

Role of capacitative Ca2+ entry in bronchial contraction and remodeling

2002 ◽  
Vol 92 (4) ◽  
pp. 1594-1602 ◽  
Author(s):  
Michele Sweeney ◽  
Sharon S. McDaniel ◽  
Oleksandr Platoshyn ◽  
Shen Zhang ◽  
Ying Yu ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Transient Receptor Potential ◽  
Bronchial Hyperresponsiveness ◽  
Receptor Potential ◽  
Transient Receptor Potential Channel ◽  
Wall Thickening ◽  
Bronchial Wall ◽  
Intracellular Ca ◽  
Transient Receptor

Asthma is characterized by airway inflammation, bronchial hyperresponsiveness, and airway obstruction by bronchospasm and bronchial wall thickening due to smooth muscle hypertrophy. A rise in cytosolic free Ca2+ concentration ([Ca2+]cyt) may serve as a shared signal transduction element that causes bronchial constriction and bronchial wall thickening in asthma. In this study, we examined whether capacitative Ca2+ entry (CCE) induced by depletion of intracellular Ca2+ stores was involved in agonist-mediated bronchial constriction and bronchial smooth muscle cell (BSMC) proliferation. In isolated bronchial rings, acetylcholine (ACh) induced a transient contraction in the absence of extracellular Ca2+ because of Ca2+ release from intracellular Ca2+ stores. Restoration of extracellular Ca2+in the presence of atropine, an M-receptor blocker, induced a further contraction that was apparently caused by a rise in [Ca2+]cyt due to CCE. In single BSMC, amplitudes of the store depletion-activated currents ( I SOC) and CCE were both enhanced when the cells proliferate, whereas chelation of extracellular Ca2+ with EGTA significantly inhibited the cell growth in the presence of serum. Furthermore, the mRNA expression of TRPC1, a transient receptor potential channel gene, was much greater in proliferating BSMC than in growth-arrested cells. Blockade of the store-operated Ca2+channels by Ni2+ decreased I SOC and CCE and markedly attenuated BSMC proliferation. These results suggest that upregulated TRPC1 expression, increased I SOC, enhanced CCE, and elevated [Ca2+]cyt may play important roles in mediating bronchial constriction and BSMC proliferation.

Regulation of intracellular calcium in N1E-115 neuroblastoma cells: the role of Na+/Ca2+exchange

2002 ◽  
Vol 282 (5) ◽  
pp. C1000-C1008 ◽  
Author(s):  
Kara L. Kopper ◽  
Joseph S. Adorante
Keyword(s):  
Membrane Potential ◽  
Intracellular Calcium ◽  
Normal Cell ◽  
Buffer Capacity ◽  
Neuroblastoma Cells ◽  
Fold Increase ◽  
Scorpion Venom ◽  
Reverse Mode ◽  
Intracellular Ca

In fura 2-loaded N1E-115 cells, regulation of intracellular Ca2+ concentration ([Ca2+]i) following a Ca2+ load induced by 1 μM thapsigargin and 10 μM carbonylcyanide p-trifluoromethyoxyphenylhydrazone (FCCP) was Na+ dependent and inhibited by 5 mM Ni2+. In cells with normal intracellular Na+ concentration ([Na+]i), removal of bath Na+, which should result in reversal of Na+/Ca2+exchange, did not increase [Ca2+]i unless cell Ca2+ buffer capacity was reduced. When N1E-115 cells were Na+ loaded using 100 μM veratridine and 4 μg/ml scorpion venom, the rate of the reverse mode of the Na+/Ca2+ exchanger was apparently enhanced, since an ∼4- to 6-fold increase in [Ca2+]ioccurred despite normal cell Ca2+ buffering. In SBFI-loaded cells, we were able to demonstrate forward operation of the Na+/Ca2+ exchanger (net efflux of Ca2+) by observing increases (∼ 6 mM) in [Na+]i. These Ni2+ (5 mM)-inhibited increases in [Na+]i could only be observed when a continuous ionomycin-induced influx of Ca2+ occurred. The voltage-sensitive dye bis-(1,3-diethylthiobarbituric acid) trimethine oxonol was used to measure changes in membrane potential. Ionomycin (1 μM) depolarized N1E-115 cells (∼25 mV). This depolarization was Na+dependent and blocked by 5 mM Ni2+ and 250–500 μM benzamil. These data provide evidence for the presence of an electrogenic Na+/Ca2+ exchanger that is capable of regulating [Ca2+]i after release of Ca2+ from cell stores.

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