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Related Concept Videos

Non-gated Ion Channels01:24

Non-gated Ion Channels

Ion channels are specialized proteins on the plasma membrane that allow charged ions to pass down their electrochemical gradient. Their main function is to maintain the membrane potential which is critical for cell viability. These channels are either gated or non-gated and can transport more than a thousand ions within milliseconds for the cellular event to occur.
Compared to the gated ion channels, the non-gated channels, also known as leakage or passive channels, have no gating mechanism.
The Nernst Equation02:59

The Nernst Equation

Nonstandard Reaction Conditions
The interconnection between standard cell potentials and various thermodynamic parameters such as the standard free energy change ΔG° and equilibrium constant K has been previously explored. For example, a redox reaction involving zinc(II) and tin(II) ions at 1 M concentration with Eºcell = +0.291 V and ΔG° = −56.2 kJ is spontaneous.
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...
Ligand-Gated Ion Channel Receptor: Gating Mechanism01:30

Ligand-Gated Ion Channel Receptor: Gating Mechanism

Ligand-gated ion channels are transmembrane proteins that play a vital role in intercellular communication and functions of the nervous system. They allow the influx of ions across the membrane once the neurotransmitter binds, allowing the subsequent transmission of electrical excitation across the neurons. Other ligand-gated ion channels, like the γ-aminobutyric acid (GABA) receptor, permit anions like chloride into the cells on the binding of the GABA molecule. Their entry into the cell...
The Resting Membrane Potential01:21

The Resting Membrane Potential

Overview
Renal Drug Excretion: Effect of Urine pH, Flow Rate, and Drug pKa01:22

Renal Drug Excretion: Effect of Urine pH, Flow Rate, and Drug pKa

The pH of urine, the drug's pKa, and the urine flow rate are vital parameters for drug reabsorption and excretion. Urinary pH varies between 4.6 and 8.0 and is influenced by diet, drug intake, and the patient's pathophysiology. It affects a drug's ionization state and reabsorption. For instance, carbohydrate-rich food produces alkaline urine promoting drug excretion, while proteins and certain medications like ascorbic acid lead to acidic urine enhancing reabsorption.
The pKa of a drug,...

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Related Experiment Video

Updated: May 11, 2026

Study of the Functions and Activities of Neuronal K-Cl Co-Transporter KCC2 Using Western Blotting
10:08

Study of the Functions and Activities of Neuronal K-Cl Co-Transporter KCC2 Using Western Blotting

Published on: December 9, 2022

Need to quickly excrete K(+)? Turn off NCC.

Alicia A McDonough1, Jang H Youn

  • 1Department of Cell and Neurobiology, Keck School of Medicine of the University of Southern California, Los Angeles, California, USA. mcdonoug@usc.edu

Kidney International
|May 2, 2013
PubMed
Summary

Dietary potassium intake rapidly increases renal potassium excretion. Researchers discovered that potassium intake dephosphorylates the kidney

Area of Science:

  • Nephrology
  • Molecular Biology
  • Physiology

Background:

  • Renal potassium (K+) excretion rapidly increases after dietary K+ intake.
  • The molecular mechanisms driving this rapid adaptation are not fully understood.

Purpose of the Study:

  • To investigate the molecular mechanisms underlying the rapid increase in renal K+ excretion following dietary K+ intake.

Main Methods:

  • The study utilized a mouse model to examine changes in the renal distal convoluted tubule NaCl cotransporter.
  • Key molecular events were monitored following dietary K+ administration.

Main Results:

  • Dietary K+ intake induced rapid and near-complete dephosphorylation of the renal distal convoluted tubule NaCl cotransporter.

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Recording of Inward Rectifying K+ Currents in Freshly Isolated Basilar Artery Smooth Muscle Cells by Patch Clamp Technique
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Last Updated: May 11, 2026

Study of the Functions and Activities of Neuronal K-Cl Co-Transporter KCC2 Using Western Blotting
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Study of the Functions and Activities of Neuronal K-Cl Co-Transporter KCC2 Using Western Blotting

Published on: December 9, 2022

Functional Characterization of Na+/H+ Exchangers of Intracellular Compartments Using Proton-killing Selection to Express Them at the Plasma Membrane
07:38

Functional Characterization of Na+/H+ Exchangers of Intracellular Compartments Using Proton-killing Selection to Express Them at the Plasma Membrane

Published on: March 30, 2015

Recording of Inward Rectifying K+ Currents in Freshly Isolated Basilar Artery Smooth Muscle Cells by Patch Clamp Technique
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Recording of Inward Rectifying K+ Currents in Freshly Isolated Basilar Artery Smooth Muscle Cells by Patch Clamp Technique

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  • This dephosphorylation was temporally associated with increased sodium (Na+) and K+ excretion.
  • The observed response was independent of aldosterone.

    • Conclusions:

    • The dephosphorylation of the renal distal convoluted tubule NaCl cotransporter is a key event in the acute adaptation to dietary K+ intake.
    • This mechanism plays a crucial role in maintaining kidney homeostasis during potassium loading.