scholarly journals GW25-e3563 Role of late sodium current in ventricular arrhythmias caused by increased intracellular calcium concentration

2014 ◽  
Vol 64 (16) ◽  
pp. C50
Author(s):  
Wei Xiaohong ◽  
Huang Sihui ◽  
Yang Qiaomei ◽  
Huo Yong ◽  
Wu Lin
Keyword(s):  
Intracellular Calcium ◽  
Ventricular Arrhythmias ◽  
Calcium Concentration ◽  
Sodium Current ◽  
Intracellular Calcium Concentration ◽  
Late Sodium Current

Abstract 14727: Late Sodium Current Plays a Role in Ventricular Arrhythmias Associated With Increased Intracellular Calcium Concentration

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Xiaohong Wei ◽  
Yong Huo ◽  
Sihui Huang ◽  
Qiaomei Yang ◽  
Lu Ren ◽  
...  
Keyword(s):  
Intracellular Calcium ◽  
Ventricular Arrhythmias ◽  
Calcium Concentration ◽  
Sodium Current ◽  
Calcium Transient ◽  
Bay K 8644 ◽  
Intracellular Calcium Concentration ◽  
Polymorphic Ventricular Tachycardia ◽  
Late Sodium Current ◽  
Multiple Channel

Objective: An increase in intracellular calcium concentration is associated with the prolongation of action potential duration (APD) and polymorphic ventricular tachycardia (PVT). Recent studies indicated that late sodium current inhibitor is effective in preventing ventricular arrhythmias in patients with long QT syndrome 8. The objective of the study was to determine the role of late sodium current in calcium related ventricular arrhythmias. Methods: Hearts from New Zealand female rabbits were perfused in a Langendorff mode. The atrioventricular nodal area was thermally ablated to produce complete atrioventricular block, and then heart was paced at stated frequency. Multiple channel monophasic action potentials (MAP) and pseudo 12-lead electrocardiograms (ECGs) were recorded. Calcium transient and myocyte contraction were determined in rabbit ventricular myocytes. Results: Bay-K 8644 (10-300 nM) increased both epi- and endo- cardial MAPD90 of left ventricle in concentration dependent manners, from (176±6) to (222±13) ms, and (201±6) to (246±10) ms (n=15, p<0.05 vs control), respectively. In the presence of 1 nM ATX-II, Bay-K 8644 caused a greater prolongation of epi-MAPD90 which was increased from (182±6) to (342±21) ms (n=9, p<0.05 vs control). The prolongation of MAPD90 caused by Bay-K 8644 were reversed by 1 μM TTX in both absence and presence of ATX-II. Additionally, the incidence of PVT evoked by Bay-K 8644 was also greater in the presence compared to the absence of ATX-II. 200 nM Bay-K 8644 caused few arrhythmias in absence of ATX-II. In contrast, PVT occurred in 7/9 (77.78%) of hearts treated with 200 nM Bay-K 8644 in the presence of ATX-II. These arrhythmias could be abolished by 1 μM TTX in the continued presence of Bay-K 8644. TTX (1 μM) attenuated the increase by 200 nM Bay-K 8644 of intracellular calcium transient and myocyte contraction amplitude by 10.8% and 14.6%, respectively (n=6, p<0.05). Conclusion: Both endogenous and enhanced late sodium current contributes to the ventricular arrhythmias with increased intracellular calcium concentration. Inhibition of late sodium current may be effective in preventing or treating calcium overload-related ventricular arrhythmias and dysfunction of myocardial contraction.

An Active Role for Astrocytes in Synaptic Plasticity?

2010 ◽  
Vol 104 (3) ◽  
pp. 1216-1218 ◽  
Author(s):  
Ian Wenker
Keyword(s):  
Synaptic Plasticity ◽  
Transgenic Mice ◽  
Intracellular Calcium ◽  
Calcium Concentration ◽  
Active Role ◽  
Intracellular Calcium Concentration ◽  
Synaptic Potentiation ◽  
Calcium Dependent

Recently, Henneberger and colleagues blocked hippocampal long-term synaptic potentiation (LTP) induction by “clamping” intracellular calcium concentration of individual CA1 astrocytes, suggesting calcium-dependent gliotransmitter release from astocytes plays a role in hippocampal LTP induction. However, using transgenic mice to manipulate astrocytic calcium, Agulhon and colleagues demonstrated no effect on LTP induction. Until the question of how intracellular calcium causes gliotransmitter release is answered, the role of astrocytes in synaptic plasticity will be incompletely understood.

PTH receptor coupling to phospholipase C is an alternate pathway of signal transduction in bone and kidney

1990 ◽  
Vol 258 (2) ◽  
pp. F223-F231 ◽  
Author(s):  
R. Dunlay ◽  
K. Hruska
Keyword(s):  
Signal Transduction ◽  
Intracellular Calcium ◽  
Phospholipase C ◽  
Calcium Concentration ◽  
Regulatory Protein ◽  
Intracellular Calcium Concentration ◽  
Calcium Stores ◽  
Base Line ◽  
Alternate Pathway

The parathyroid hormone (PTH) receptor is coupled via a guanine nucleotide-binding regulatory protein (G protein) to phospholipase C (PLC). Binding of PTH to its receptor leads to activation of PLC with the subsequent hydrolysis of phosphatidylinositol 4,5-bisphosphate to inositol 1,4,5-trisphosphate (IP3) and diacylglycerol (DAG). IP3 generation leads to the release of intracellular calcium stores, which produces an increase in the intracellular calcium concentration. DAG activates protein kinase C (PKC). Both IP3 metabolites and PKC may play a role in returning the intracellular calcium concentration back to base line, by stimulating the movement of calcium from the intracellular to the extracellular compartment, as well as by sequestering calcium within intracellular organelles. PKC appears to be important in the development of desensitization and downregulation of the PTH receptor to PTH. Activation of PLC may be important in modulating the well-known effects of PTH on bone and kidney and also may be relevant to recently described actions, such as the possible role of PTH as a growth factor in skeletal tissue. Important issues that need to be addressed in this field include 1) characterization of the PTH receptor, 2) the possible role of low-molecular-weight G proteins in PTH signal transduction, and 3) further description of the role of alternate pathway signal transduction in producing the effects of PTH.

Intracellular calcium levels in the Plasmodium berghei ookinete

Parasitology ◽  
2008 ◽  
Vol 135 (12) ◽  
pp. 1355-1362 ◽  
Author(s):  
I. SIDÉN-KIAMOS ◽  
C. LOUIS
Keyword(s):  
Intracellular Calcium ◽  
Plasmodium Berghei ◽  
Calcium Concentration ◽  
Insect Cells ◽  
Ionophore A23187 ◽  
Rodent Malaria Parasite ◽  
Calcium Indicators ◽  
Intracellular Ca

SUMMARYOokinetes are the motile and invasive stages of Plasmodium parasites in the mosquito host. Here we explore the role of intracellular Ca2+ in ookinete survival and motility as well as in the formation of oocysts in vitro in the rodent malaria parasite Plasmodium berghei. Treatment with the Ca2+ ionophore A23187 induced death of the parasite, an effect that could be prevented if the ookinetes were co-incubated with insect cells before incubation with the ionophore. Treatment with the intracellular calcium chelator BAPTA/AM resulted in increased formation of oocysts in vitro. Calcium imaging in the ookinete using fluorescent calcium indicators revealed that the purified ookinetes have an intracellular calcium concentration in the range of 100 nm. Intracellular calcium levels decreased substantially when the ookinetes were incubated with insect cells and their motility was concomitantly increased. Our results suggest a pleiotropic role for intracellular calcium in the ookinete.

Sign in / Sign up

Export Citation Format

Share Document