The proper intracellular Ca(2+) signaling is essential for normal cell functions and organ development, and the maintaining Ca(2+) homeostasis in cardiac myocytes is of functional importance for the intact heart. As the first functional organ in the vertebrate embryo, the heart is continuously remodeled and maintains its physiologic pumping function in response to increasing circulatory demands. The expressions of Ca(2+) handing proteins in the embryonic heart, however, are different from those in neonatal and adult hearts, which means that the regulation of Ca(2+) transients in embryonic cardiomyocytes is different from that in adult cardiac myocytes. Recent advances in molecular and cellular biology, as well as the application of embryonic stem cell differentiation system, have made progress in uncovering the regulation of Ca(2+) homeostasis during cardiomyogenesis. This paper briefly summarizes the Ca(2+) homeostasis during early development of cardiomyocytes and reviews current knowledge of the regulatory mechanisms controlling Ca(2+) homeostasis during cardiomyocyte development.
Calcium ; physiology ; Calcium Channels ; metabolism ; physiology ; Calcium Signaling ; Heart ; embryology ; Homeostasis ; physiology ; Humans ; Intracellular Fluid ; physiology ; Myocytes, Cardiac ; metabolism ; physiology

No abstract available.
Animal ; Calcium Signaling/physiology* ; Exocytosis/physiology ; Pancreas/physiology* ; Pancreas/cytology

Sixty years elapsed since Chang (Hsiang-Tung Chang, Xiang-Tong Zhang) presented his seminal report "Cortical neurons with particular reference to the apical dendrite" at the Cold Spring Harbor Symposium. Thanks to the development of elaborated techniques through the 6 decades, our understanding of the dendrite has been pushed forward greatly: the backward and forward conductions during excitation, sodium and calcium conductances, chemical excitation by uncaging glutamate at a dimension of micrometer, and the quantitative study of chemical organization of postsynaptic density (PSD), etc. Though the progression is great, there are still tough problems in dendritic research, especially the integration through dendritic spine.
Calcium Signaling ; Dendrites ; physiology ; Glutamic Acid ; metabolism

Exogenous calcium can enhance the resistance of certain plants to abiotic stress. Research have demonstrated that exogenous calcium could enhances the resistance of honeysuckle under salt stress by promoting the transmission of photosynthetic electrons.The aim of this study was to investigate the effects of exogenous calcium on the contents of Na~+,K~+,Ca~(2+),Mg~(2+)and the expression of photosynthetic related genes Cab and rbc L. In this study,we used ICP-OES to analysis ion contents and used qRT-PCR to analysis the expression patterns of Cab and rbc L. The results showed that CaCl_2 significantly enhanced the K~+-Na~+,Ca~(2+)-Na~+,Mg~(2+)-Na+ratio of honeysuckle treated with 50 and 100 mmol·L~(-1) NaCl. Meanwhile,Cab and rbc L were significantly up-regulated under short-term salt stress,and CaCl_2 promoted this trend. From the two gene expression patterns,rbc L rapidly up-regulated on the first day of stress and then decreased,and was more sensitive to environmental changes. In summary,exogenous calcium could alleviate salt stress and increase plant development by increasing intracellular K~+-Na~+,Ca~(2+)-Na~+,Mg~(2+)-Na+ratio,and the transient overexpression of Cab and rbc L.
Calcium ; physiology ; Cations ; analysis ; Lonicera ; physiology ; Photosynthesis ; Salt Stress

It has been shown that mitochondria not only control their own Ca(2+) concentration ([Ca(2+)]), but also exert an influence over Ca(2+) signaling of the entire cell, including the endoplasmic reticulum or the sarcoplasmic reticulum, the plasma membrane, and the nucleus. That is to say, mitochondria couple cellular metabolic state with Ca(2+) transport processes. This review focuses on the ways in which the mitochondrial Ca(2+) handling system provides integrity and modulation for the cell to cope with the complex actions throughout its life cycle, enumerates some indeterminate aspects about it, and finally, prospects directions of future research.
Biological Transport ; Calcium Signaling ; Cell Membrane ; physiology ; Endoplasmic Reticulum ; physiology ; Mitochondria ; physiology ; Sarcoplasmic Reticulum ; physiology

As an important intracellular messenger, Ca2+ plays a major role in sperm motility. In spermatozoa, multiple Ca2(+)-permeable channels have been identified in the plasma membrane of mammalian sperm, including voltage-gated Ca2+ channels (Cav channels), cyclic nucleotide-gated channels (CNGC), cation channels of sperm (CatSper) and the transient receptor potential (TRP) family. As calcium regulation of sperm motility is mainly mediated by these calcium channels, any aberration of the channels can lead to the decline of sperm activities. Recent progress in the researches on the relationship between sperm motility and calcium-related ion channels is briefly reviewed in this article.
Animals ; Calcium ; metabolism ; Calcium Channels ; Male ; Sperm Motility ; physiology ; Spermatozoa ; physiology

Calcium ion exists extensively in cells as the second messenger, and calcium channel blocker (CCB) is widely used to treat cardiac, skeletal muscular diseases. With the advances in the investigation of human sperm calcium channel, CCB has been proved to affect not only the shape, activation and acrosome reaction, but also the function of human sperm, which may afford a new approach to male contraception.
Calcium Channel Blockers ; pharmacology ; Calcium Channels ; physiology ; Humans ; Male ; Spermatozoa ; drug effects ; physiology

Contraction of smooth muscle cells is triggered by an increase in cytosolic Ca(2+) upon agonist stimulation. Ca(2+) influx across the plasma membrane constitutes a major component of the agonist-induced response in smooth muscle cells. Traditionally, voltage-operated Ca(2+) channel (VOCC) is considered as the channel mediating the Ca(2+) entry. However, this view has been challenged by recent discoveries, which demonstrated that other types of ion channels, such as store-operated and/or receptor-operated Ca(2+) channels (SOCC and/or ROCC), also participate in Ca(2+) response induced by agonists in smooth muscle cells. SOCC is defined as the channel activated in response to the depletion of the internal Ca(2+) stores, an event secondary to G protein coupled receptor or receptor tyrosine kinase stimulation. The Ca(2+) flow mediated by SOCC is termed as capacitative Ca(2+) entry (CCE). Previous study from other group has demonstrated that VOCC played a predominant role in ACh-induced contraction of distal colon smooth muscle in guinea pig. However, whether SOCC participates in the agonist-induced contractile response in this particular tissue is unknown. The present study was performed to investigate the role of CCE in ACh-induced mechanical activity of distal colon smooth muscle in rats. The contractile function of the smooth muscle was assessed by measuring isometric force of isolated rat distal colon rings. We showed that both high extracellular K(+) (40 mmol/L) and ACh (5 mumol/L) evoked striking contraction of the smooth muscle. The contractile responses were almost abolished by removal of extracellular Ca(2+) with ethylene glycol-bis(2-aminoethylether)-N,N,N',N' tetraacetic acid (EGTA), suggesting a critical contribution of extracellular source of Ca(2+) to the contraction. Verapamil (5 mumol/L), an L-type VOCC blocker, significantly attenuated, but didn't completely eliminate the high K(+)- and ACh-induced contraction (74% and 41% for high K(+) and ACh, respectively), indicating that additional channels might be involved in the contractile mechanism. Furthermore, ACh only induced transient contractions in the absence of extracellular Ca(2+). Readmission of Ca(2+) into the extracellular compartment resulted in a significant and sustained increase in the tension of the smooth muscle. This response was not affected by verapamil (5 mumol/L) and Cd(2+) (5 mumol/L), both of which efficiently block VOCC at the doses. However, La(3+), a known inhibitor of SOCC, significantly suppressed the Ca(2+) readdition-induced contraction in a dose-dependent manner. On the basis of these results, we conclude that contraction of smooth muscle in the distal colon is regulated by multiple Ca(2+) channels. In addition to VOCC-mediated Ca(2+) influx, SOCC-mediated CCE participates in agonist-induced contractile response of distal colon smooth muscle in rats.
Acetylcholine ; physiology ; Animals ; Calcium ; metabolism ; Calcium Channels ; physiology ; Colon ; physiology ; Female ; Male ; Muscle Contraction ; physiology ; Muscle, Smooth ; physiology ; Myocytes, Smooth Muscle ; physiology ; Rats ; Rats, Sprague-Dawley ; Verapamil ; pharmacology

The purpose of this study is to identify the electrical activity of neuron, the existence of the transition from bursting pattern to spiking pattern and the ion mechanism of the bursting pattern. The intracellular electrical activity patterns of single neurons in the stomatogastric ganglion (STG) of crayfish were recorded when the extracellular calcium concentration ([Ca(2+)](o)) or calcium-dependent potassium channel blocker tetraethylammonium concentration ([TEA](o)) were changed, using intracellular recording method. These single neurons were also functionally isolated from the ganglion by application of atropine and picrotoxin which could block the inhibitory acetylcholine synapses and glutamatergic synapses respectively. When [Ca(2+)](o) was decreased by increasing EGTA, the membrane potential of the neuron was increased, and the electrical activity patterns were changed from the resting state with lower potential value (resting state of polarization) to the bursting pattern firstly, and then to the spiking pattern, at last to the resting state with higher potential value (resting state of depolarization). When [TEA](o) was increased, the membrane potential of the neuron was increased, and the electrical activity pattern was changed from the resting state with lower potential value (resting state of polarization) to the bursting pattern firstly, and then to the spiking pattern. The duration of the burst of the bursting pattern was increased. When [Ca(2+)](o) was increased or [TEA](o) was decreased, an inverse procedure of the electrical activity pattern was exhibited. On one hand, the results indicate that a single neuron can generate various electrical activity patterns corresponding to different physiological conditions, and the regularity of the transitions between different electrical activity patterns. On the other hand, the results identify that the initiation and termination of the burst in bursting pattern are determined by calcium-activated potassium conductance, which is adjusted by intracellular calcium concentration influenced by inward calcium current. It may be the ionic mechanism of generation of the bursting pattern in a single neuron.
Action Potentials ; physiology ; Animals ; Astacoidea ; physiology ; Calcium ; metabolism ; Calcium Channels ; metabolism ; Ganglia, Invertebrate ; physiology ; Neurons ; physiology ; Potassium Channels, Calcium-Activated ; metabolism

Sodium calcium exchanger (NCX), which is widely expressed in the plasma membrane, mitochondrial membrane and secretory vesicles in diverse kinds of cells, belongs to a type of cation translocators. NCX works in two modes, the forward mode and reverse mode, to regulate the intracellular Ca(2+) concentration bi-directionally. In the forward mode, NCX carries Ca(2+) out of the cell against its electrochemical gradients coupled to the influx of Na(+) down its electrochemical gradients; alternatively, Ca(2+) enters through the reverse mode of NCX, and Na(+) is carried out of the cell. Exactly through the two-way modes, NCX can regulate intracellular Ca(2+) concentration fleetly and accurately, and plays a critical role in a series of physiological processes including intracellular signal transduction, growth and development of cells, excitation and its coupled functions of excitable cells. NCX are acknowledged to be involved in myofiber contraction, neurotransmission, migration and differentiation of neurogliocyte, activation of immune cells, secretion of cytokines and hormones etc. Moreover, abnormal activation of the reverse mode of NCX plays a vital role in many pathological processes including cell apoptosis, ischemia-reperfusion injury, insulin secretion, tumor etc. Here we reviewed the research status about the NCX's participation in some physiological and pathophysiological processes, so as to provide comprehensive understanding about its functions.
Animals ; Apoptosis ; Calcium ; physiology ; Humans ; Ion Transport ; Reperfusion Injury ; physiopathology ; Signal Transduction ; Sodium ; physiology ; Sodium-Calcium Exchanger ; physiology