Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Accessory Structures of the Skin: Sweat Glands01:20

Accessory Structures of the Skin: Sweat Glands

Sweat glands or sudoriferous glands are one of the important accessory structures of the skin. They are small, coiled tubular structures located in the dermis, the middle layer of the skin. Sweat glands are responsible for producing and secreting sweat, a watery fluid that helps regulate body temperature and excrete waste products.
Sweat glands are classified as merocrine glands; that is, the secretions are excreted by exocytosis through a duct without affecting the cells of the gland. There...
Antihypertensive Drugs: Action of β1 Blockers01:17

Antihypertensive Drugs: Action of β1 Blockers

β1-receptors are primarily located in the heart and kidneys. In cardiac myocytes, these receptors interact with neurotransmitters released by the sympathetic nervous system during heightened activity or danger. As a result, β1-receptors get activated, initiating a series of biochemical processes. Excessive activation of beta receptors due to chronic stress can abnormally increase heart rate and contractility, resulting in high blood pressure or hypertension. To counteract this, β1-blockers...
Adrenergic Receptors: β Subtype01:26

Adrenergic Receptors: β Subtype

β-adrenoceptors have varied sensitivities towards adrenaline, noradrenaline, and isoprenaline. The order of agonist potency is as follows:
Isoprenaline > Adrenaline > Noradrenaline
Neurotransmitter binding to these receptors causes activation of adenylyl cyclase resulting in increased concentrations of cAMP and modulation of calcium ion channels within the cell. They are further classified into β1, β2, and β3 subtypes.
β1-adrenoceptors: β1-adrenoceptors have equal affinities for...
Adrenergic Antagonists: Pharmacological Actions of β-Receptor Blockers01:27

Adrenergic Antagonists: Pharmacological Actions of β-Receptor Blockers

β-receptor blockers significantly impact the cardiovascular system by counteracting catecholamine-induced sympathetic responses. These medications decrease heart rate, contractility, and cardiac output, potentially leading to cardiac depression, life-threatening bradycardia, and death. Therapeutically, β-blockers function as mild antihypertensives and are utilized in treating angina pectoris and cardiac arrhythmias. However, nonselective β-blockers inhibit β2-receptors in bronchial smooth...
Antihypertensive Drugs: Types of β-Blockers01:28

Antihypertensive Drugs: Types of β-Blockers

β receptors are classified into three subclasses: β1, β2, and β3. β1 receptors are primarily located in the heart and kidneys. When they get activated, they increase heart rate, contractility, and renin release. This process enhances blood pressure and aids in stress management. In contrast, β2 receptors are situated mainly in the lungs, blood vessels, and skeletal muscles. Upon activation, they trigger smooth muscle relaxation, causing bronchodilation and vasodilation. This widens airways and...
Sympathetic Activation01:16

Sympathetic Activation

The sympathetic division can influence tissues and organs by releasing norepinephrine at peripheral synapses and distributing epinephrine and norepinephrine through the bloodstream. In times of crisis or stress, sympathetic activation occurs, which is regulated by sympathetic centers in the hypothalamus. As a result, sympathetic activation prepares the body for physical exertion, rapid ATP production, and heightened alertness, allowing individuals to respond effectively to challenging or...

You might also read

Related Articles

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

Sort by
Same author

Post Hoc Analysis of Recombinant C1 Inhibitor Clinical Data Using Contemporary Endpoints for Hereditary Angioedema.

Advances in therapy·2026
Same author

Comparative Efficacy of Recombinant C1 Inhibitor Versus Sebetralstat for On-Demand Treatment of Hereditary Angioedema Attacks: A Matching-Adjusted Indirect Treatment Comparison.

Advances in therapy·2026
Same author

Artificial intelligence models for point-of-care ultrasound diagnostics in dogs.

Frontiers in veterinary science·2026
Same author

Non-negotiables in digital health innovation: leadership perspectives from the C-suite.

BMJ leader·2026
Same author

Patient-reported disease burden and health care utilization of HAE-nl-C1INH: insights from a real-world survey.

Clinical and experimental medicine·2026
Same author

Preliminary Evidence for a Western Blot Diagnosis of Satoyoshi Syndrome Using SH-SY5Y Neuroblastoma Cell Lysate as the Antigen Source.

Diagnostics (Basel, Switzerland)·2025

Related Experiment Video

Updated: May 21, 2026

Use of Galvanic Skin Responses, Salivary Biomarkers, and Self-reports to Assess Undergraduate Student Performance During a Laboratory Exam Activity
07:32

Use of Galvanic Skin Responses, Salivary Biomarkers, and Self-reports to Assess Undergraduate Student Performance During a Laboratory Exam Activity

Published on: February 10, 2016

Blocking the beta-adrenergic system does not affect sweat gland function during heat acclimation.

Ricardo Martinez1, Douglas Jones, Daniel Hodge

  • 1School of Exercise and Nutritional Sciences, San Diego State University, San Diego, CA 92182-7251, USA.

Autonomic Neuroscience : Basic & Clinical
|June 20, 2012
PubMed
Summary

Beta-adrenergic innervation does not enhance sweat production in humans after heat acclimation. This study found no significant difference in sweat rates between inhibited and control arms, questioning its physiological role.

More Related Videos

Determining Basal Energy Expenditure and the Capacity of Thermogenic Adipocytes to Expend Energy in Obese Mice
06:57

Determining Basal Energy Expenditure and the Capacity of Thermogenic Adipocytes to Expend Energy in Obese Mice

Published on: November 11, 2021

Disrupting Reconsolidation of Fear Memory in Humans by a Noradrenergic β-Blocker
08:32

Disrupting Reconsolidation of Fear Memory in Humans by a Noradrenergic β-Blocker

Published on: December 18, 2014

Related Experiment Videos

Last Updated: May 21, 2026

Use of Galvanic Skin Responses, Salivary Biomarkers, and Self-reports to Assess Undergraduate Student Performance During a Laboratory Exam Activity
07:32

Use of Galvanic Skin Responses, Salivary Biomarkers, and Self-reports to Assess Undergraduate Student Performance During a Laboratory Exam Activity

Published on: February 10, 2016

Determining Basal Energy Expenditure and the Capacity of Thermogenic Adipocytes to Expend Energy in Obese Mice
06:57

Determining Basal Energy Expenditure and the Capacity of Thermogenic Adipocytes to Expend Energy in Obese Mice

Published on: November 11, 2021

Disrupting Reconsolidation of Fear Memory in Humans by a Noradrenergic β-Blocker
08:32

Disrupting Reconsolidation of Fear Memory in Humans by a Noradrenergic β-Blocker

Published on: December 18, 2014

Area of Science:

  • Human physiology
  • Thermoregulation
  • Sweat gland function

Background:

  • Eccrine sweat glands are crucial for thermoregulation.
  • Innervation of sweat glands involves both cholinergic and adrenergic pathways.
  • The specific role of beta-adrenergic innervation in eccrine sweat production during heat acclimation is not fully understood.

Purpose of the Study:

  • To investigate the hypothesis that beta-adrenergic innervation enhances sweat production in human eccrine sweat glands following heat acclimation.
  • To determine the physiological significance of adrenergic innervation in eccrine sweat glands.

Main Methods:

  • Eight healthy subjects underwent 8 days of active heat acclimation.
  • Beta-adrenergic blockade was achieved using propranolol via iontophoresis on one forearm.
  • A saline solution was used as a control on the opposing forearm.
  • Sweat rates were measured during exercise in a controlled environmental chamber.

Main Results:

  • No significant difference in mean sweat rate was observed between the propranolol-inhibited forearm (0.47 ± 0.30 mg/cm(2)/min) and the control forearm (0.44 ± 0.25 mg/cm(2)/min) after heat acclimation.
  • The findings do not support the hypothesis that beta-adrenergic innervation facilitates eccrine sweat gland function during heat acclimation.

Conclusions:

  • Beta-adrenergic innervation does not appear to play a significant role in facilitating eccrine sweat production following heat acclimation in humans.
  • The physiological importance of the dual cholinergic and adrenergic innervation of eccrine sweat glands requires further investigation.