Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Smooth Muscle Contraction

Smooth Muscle Contraction

Smooth muscle contraction is a complex process vital for various bodily functions, from maintaining blood vessel tension to facilitating the movement of food through the digestive tract. Unlike striated muscles, smooth muscle contraction begins more slowly and lasts longer.
The onset of contraction is triggered by an increase in calcium ions within the sarcoplasm, similar to the process in striated muscle. However, smooth muscles have a relatively smaller reservoir of the sarcoplasmic...

Relaxation of Skeletal Muscles

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.

Peripherally and Centrally Acting Muscle Relaxants: A Comparison

Peripherally and Centrally Acting Muscle Relaxants: A Comparison

Skeletal muscle relaxants can target the central nervous system [CNS] to reduce muscle tension or act directly at the neuromuscular junction to induce temporary paralysis. These two classes of muscle relaxants are called centrally acting muscle relaxants and peripherally acting muscle relaxants. They differ in their action, mechanism, administration route, and clinical uses.
Centrally acting muscle relaxants can be further divided into spasmolytic and antispasmodic drugs. Spasmolytic drugs,...

Antihypertensive Drugs: Action of Calcium Channel Blockers

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,...

Centrally Acting Muscle Relaxants: Therapeutic Uses

Centrally Acting Muscle Relaxants: Therapeutic Uses

Centrally acting muscle relaxants reduce muscle tone and tension by interfering with the postsynaptic reflexes in the central nervous system.
Centrally acting drugs are classified into spasmolytic and antispasmodic drugs. Spasmolytic drugs such as baclofen, diazepam, and tizanidine inhibit spinal motor neurons and decrease muscle tone. Spasmolytic drugs are administered for severe and chronic spasms due to multiple sclerosis, cerebral palsy, stroke, and spinal cord and muscle injuries. However,...

Direct-Acting Cholinergic Agonists: Pharmacological Actions

Direct-Acting Cholinergic Agonists: Pharmacological Actions

Direct-acting cholinergic agonists exert their pharmacological actions by mimicking the effects of acetylcholine on postsynaptic muscarinic receptors to generate parasympathetic responses. These agents elicit a range of physiological responses, including cardiovascular effects. For example, activation of muscarinic receptors induces bradycardia, decreased cardiac output, reduced peripheral resistance, and consequent hypotension. In the eye, stimulation of M3 receptors leads to smooth muscle...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Myeloid-specific Exoc5 deficiency develops renal inflammation and hypertension.

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie·2026

Same author

Expanding diverse horizons in smooth muscle research: a symposium review of "Muscle and Pathology/Health: Frontiers of Translational Research" at the 66th Annual Meeting of Japan Society of Smooth Muscle Research.

Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi·2025

Same author

Anti-ST2 antibody reduces airway hyperresponsiveness mediated by monocyte-derived macrophages during influenza A infection.

Mucosal immunology·2025

Same author

Rediscovery of PHI-1/PPP1R14B: Emerging Roles of Cellular PP1 Signaling Mediated by the <i>PPP1R14B</i> Gene Product in Multiple Cancers and Beyond.

Biomolecules·2025

Same author

Molecular characterization of feline caliciviruses isolated from several adult cats with atypical infection showing severe flu-like symptoms on a remote island in Ehime, Japan.

Virus research·2025

Same author

An accelerometry-based, low cost and non-invasive respiration monitoring in anesthetized mice.

The Journal of veterinary medical science·2025

Search research articles

Related Experiment Video

Updated: May 21, 2026

Bladder Smooth Muscle Strip Contractility as a Method to Evaluate Lower Urinary Tract Pharmacology

Bladder Smooth Muscle Strip Contractility as a Method to Evaluate Lower Urinary Tract Pharmacology

Published on: August 18, 2014

Caffeine relaxes smooth muscle through actin depolymerization.

Tracy Tazzeo¹, Genevieve Bates, Horia Nicolae Roman

¹Firestone Institute for Respiratory Health, St. Joseph’s Hospital and the Department of Medicine, McMaster University, Hamilton, Ontario, Canada.

American Journal of Physiology. Lung Cellular and Molecular Physiology

|June 12, 2012

Summary

Caffeine interferes with smooth muscle contraction by disrupting actin filament binding, not just calcium release. This novel mechanism impacts cell physiology studies using caffeine.

More Related Videos

Mesenteric Artery Contraction and Relaxation Studies Using Automated Wire Myography

Mesenteric Artery Contraction and Relaxation Studies Using Automated Wire Myography

Published on: September 22, 2011

Measurement of Smooth Muscle Function in the Isolated Tissue Bath-applications to Pharmacology Research

Measurement of Smooth Muscle Function in the Isolated Tissue Bath-applications to Pharmacology Research

Published on: January 19, 2015

Related Experiment Videos

Last Updated: May 21, 2026

Bladder Smooth Muscle Strip Contractility as a Method to Evaluate Lower Urinary Tract Pharmacology

Bladder Smooth Muscle Strip Contractility as a Method to Evaluate Lower Urinary Tract Pharmacology

Published on: August 18, 2014

Mesenteric Artery Contraction and Relaxation Studies Using Automated Wire Myography

Mesenteric Artery Contraction and Relaxation Studies Using Automated Wire Myography

Published on: September 22, 2011

Measurement of Smooth Muscle Function in the Isolated Tissue Bath-applications to Pharmacology Research

Measurement of Smooth Muscle Function in the Isolated Tissue Bath-applications to Pharmacology Research

Published on: January 19, 2015

Area of Science:

Cell Physiology
Smooth Muscle Biology
Pharmacology

Background:

Caffeine is commonly used to study calcium (Ca2+) release in cell physiology.
A novel mechanism of caffeine action beyond Ca2+ release has been investigated.

Purpose of the Study:

To elucidate the previously undescribed mechanism of caffeine action in smooth muscle.
To determine if caffeine affects the contractile apparatus independently of calcium release.

Main Methods:

Ruled out phosphodiesterase (PDE) inhibition and bitter taste receptor agonism.
Utilized beta-escin permeabilization and A23187 to deplete intracellular Ca2+ stores.
Employed molecular techniques to assess effects on myosin light chain (MLC) phosphorylation and actin-myosin interactions.

Main Results:

Caffeine reversed Ca2+-evoked tone after internal Ca2+ depletion.
Caffeine did not affect key phosphorylation or phosphatase activities involved in contraction.
Caffeine decreased actin filament binding to phosphorylated myosin and increased globular actin.

Conclusions:

Caffeine interferes with smooth muscle contraction by directly impacting actin filament function.
This actin-disrupting effect, including decreased myosin binding and potential depolymerization, is a novel finding.
Researchers using caffeine to study excitation-contraction coupling in smooth muscle should consider this actin-related mechanism.