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Related Concept Videos

The Resting Membrane Potential01:21

The Resting Membrane Potential

Overview
Resting Membrane Potential01:24

Resting Membrane Potential

The relative difference in electrical charge, or voltage, between the inside and the outside of a cell membrane, is called the membrane potential. It is generated by differences in permeability of the membrane to various ions and the concentrations of these ions across the membrane.
The Inside of a Neuron is More Negative
The membrane potential of a cell can be measured by inserting a microelectrode into a cell and comparing the charge to a reference electrode in the extracellular fluid. The...
Feedback Regulation of Calcium Concentration01:27

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Calcium is an essential signaling molecule required for various cellular functions. Calcium pumps and ion channels on cell and organellar membranes, such as those on the endoplasmic reticulum (ER), regulate calcium concentrations inside the cell. They remain closed, keeping the cytosolic calcium levels low at a resting state.
Various transmembrane receptors, such as G protein-coupled receptors (GPCRs), elicit a response to extracellular signals by increasing cytosolic calcium. Activated GPCRs...
Generation of Action Potential in Skeletal Muscles01:24

Generation of Action Potential in Skeletal Muscles

Every cell in the body maintains a membrane potential due to an uneven distribution of positive and negative charges across its plasma membrane. The membrane potential is measured in millivolts and quantifies the difference in charge across the membrane.
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Relaxation of Skeletal Muscles01:29

Relaxation of Skeletal Muscles

The period of muscle contraction primarily influences the duration of stimulation at the neuromuscular junction (NMJ), the presence of free calcium ions in the sarcoplasm, and the availability of energy or ATP to support contractions.
When an action potential reaches the axon terminal, it depolarizes the membrane and opens voltage-gated sodium channels. Sodium ions enter the cell, further depolarizing the presynaptic membrane. This depolarization causes voltage-gated calcium channels to open.
Antihypertensive Drugs: Action of Calcium Channel Blockers01:18

Antihypertensive Drugs: Action of Calcium Channel Blockers

Calcium ions are essential to contract smooth muscle cells in blood vessels. They enter these cells through voltage-dependent calcium channels, specifically L-type calcium channels in the cell membrane. These L-type calcium channels are integral to the excitation-contraction coupling process in smooth muscle. When a stimulus is received by smooth muscle cells, their membrane depolarizes. This alteration in membrane potential instigates the opening of L-type calcium channels. As a result,...

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Related Experiment Video

Updated: Jun 23, 2026

Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents
10:53

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Published on: July 3, 2013

Decrease in the transmembrane sodium activity gradient in ferret papillary muscle as a prerequisite to the calcium

T Guarnieri1

  • 1Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205.

The Journal of Clinical Investigation
|June 1, 1988
PubMed
Summary
This summary is machine-generated.

Sodium loading during calcium-free periods is crucial for calcium paradox damage. Blocking sodium entry prevents this reperfusion injury, highlighting sodium-dependent calcium exchange as a key mediator.

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Last Updated: Jun 23, 2026

Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents
10:53

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Published on: July 3, 2013

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Isolating Myofibrils from Skeletal Muscle Biopsies and Determining Contractile Function with a Nano-Newton Resolution Force Transducer
07:55

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Published on: May 7, 2020

Area of Science:

  • Cardiology
  • Cell Physiology
  • Biochemistry

Background:

  • The calcium paradox is a phenomenon of reperfusion injury.
  • Sodium-dependent calcium exchange is a potential mediator of this damage.

Purpose of the Study:

  • To investigate the role of intracellular sodium activity in mediating calcium paradox during reperfusion.
  • To identify mechanisms of sodium entry during calcium-free periods.

Main Methods:

  • Isolated ferret papillary muscles were used.
  • Intracellular sodium activity was measured using ion-selective electrodes.
  • Effects of various blockers and sodium substitution were assessed.

Main Results:

  • Intracellular sodium activity significantly increased during calcium-free periods.
  • Calcium reinstitution led to contracture, related to sodium loading.
  • Nitrendipine, tetrodotoxin, and low amiloride did not block sodium entry.
  • High amiloride or lithium substitution prevented sodium increase and paradox.

Conclusions:

  • Sodium loading is a necessary prerequisite for the calcium paradox.
  • Sodium-dependent calcium exchange is a key mechanism in this process.
  • Blocking sodium entry can prevent reperfusion injury associated with the calcium paradox.