Related Experiment Video

Updated: Jul 15, 2026

Mechanical Stimulation-induced Calcium Wave Propagation in Cell Monolayers: The Example of Bovine Corneal Endothelial Cells
10:46

Mechanical Stimulation-induced Calcium Wave Propagation in Cell Monolayers: The Example of Bovine Corneal Endothelial Cells

Published on: July 16, 2013

Effect of motilin and erythromycin on calcium-activated potassium channels in rabbit colonic myocytes

G Lu1, M G Sarr, J H Szurszewski

  • 1Department of Physiology and Biophysics, Mayo Clinic and Mayo Foundation, Rochester, Minnesota 55905, USA.

Gastroenterology
|April 18, 1998
PubMed
Abstract

Insights

Motilin and erythromycin activate calcium-activated potassium (KCa) channels in gastrointestinal smooth muscle. This activation, possibly via a second messenger system, may explain their prokinetic effects.

Area of Science:

  • Gastroenterology
  • Molecular Pharmacology
  • Ion Channel Physiology

Background:

  • Motilin and erythromycin are prokinetic agents.
  • They act on the same receptor in gastrointestinal smooth muscle.
  • Both agonists increase outward current and smooth muscle contraction.

Purpose of the Study:

  • To determine if motilin and erythromycin activate calcium-activated potassium (KCa) channels.
  • Investigate the mechanism of action of these prokinetic agents.

Main Methods:

  • Patch clamp recording techniques were used.
  • Whole-cell outward current and single-channel activity were measured.
  • Longitudinal smooth muscle cells from rabbit colon were utilized.

Main Results:

  • Erythromycin and motilin increased calcium-dependent outward potassium current.
  • Both agonists enhanced the open probability of KCa channels in cell-attached patches.

Conclusions:

  • Erythromycin and motilin activate KCa channels.
  • Activation occurs through an intracellular second messenger system.
  • This mechanism may modulate the prokinetic effect of these agonists.

More Related Videos

Contractility Measurements of Human Uterine Smooth Muscle to Aid Drug Development07:56

Contractility Measurements of Human Uterine Smooth Muscle to Aid Drug Development

Published on: January 26, 2018

Functional Characterization of Endogenously Expressed Human RYR1 Variants07:59

Functional Characterization of Endogenously Expressed Human RYR1 Variants

Published on: June 9, 2021

Related Concept Videos

Feedback Regulation of Calcium Concentration01:27

Feedback Regulation of Calcium Concentration

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...
Calmodulin-dependent Signaling01:16

Calmodulin-dependent Signaling

Calmodulin (CaM) is a calcium-binding protein in eukaryotes that controls various calcium-regulated cellular processes. It has four calcium-binding sites that bind calcium to form the calcium-calmodulin ( Ca2+-CaM) complex. GPCR stimulation increases the calcium levels in the cells that bind to CaM and induces a conformational change.
The Ca2+-CaM complex does not have enzymatic activity by itself. Instead, the complex binds downstream target proteins, including membrane proteins or enzymes,...
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,...
Antiarrhythmic Drugs: Class IV Agents as Calcium Channel Blockers01:20

Antiarrhythmic Drugs: Class IV Agents as Calcium Channel Blockers

Class IV antiarrhythmic drugs, such as verapamil and diltiazem, block calcium channels. They primarily affect the heart, slowing the conduction in calcium-dependent tissues like the SA and AV nodes. These drugs manage reentrant supraventricular tachycardia (SVT) and reduce ventricular rate in atrial flutter/fibrillation.
Verapamil, a calcium channel blocker, inhibits calcium movement across myocardial cell membranes and vascular smooth muscle. This results in the dilation of coronary and...
Drugs Affecting GI Tract Motility: Serotonin Receptor Agonists01:23

Drugs Affecting GI Tract Motility: Serotonin Receptor Agonists

Serotonin, a crucial neurotransmitter synthesized by enterochromaffin cells, plays a cardinal role in regulating gastrointestinal (GI) motility. With over 90% of the body's total serotonin in the GI tract, its influence on digestive processes is profound. Serotonin is swiftly released upon various stimuli, such as food boluses or certain drugs, triggering intrinsic sensory neurons in the myenteric plexus and extrinsic vagal and spinal sensory neurons. This leads to the activation of the...