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

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 Neurons: Neurotransmission01:27

Adrenergic Neurons: Neurotransmission

Postganglionic sympathetic fibers (except those supplying the sweat glands) releasing noradrenaline or norepinephrine are called noradrenergic or adrenergic neurons. Noradrenaline, dopamine, adrenaline, or epinephrine are collectively called "catecholamines" as they contain a catechol moiety and an amine side chain. The five stages of neurotransmitter release involve their synthesis, storage, release, reuptake and metabolism.
Synthesis: Catecholamine synthesis requires tyrosine, which is taken...
Adrenergic Receptors: ɑ Subtype01:31

Adrenergic Receptors: ɑ Subtype

Adrenoceptors are classified into α and ꞵ classes based on their potencies to catecholamine agonists. α-adrenoceptors show the following order of catecholamine potency:
Adrenaline ≥ Noradrenaline >> Isoprenaline
α-adrenoceptors are further divided into α1 and α2-adrenoceptors.
α1-Adrenoceptors: These receptors are located postsynaptically on the effector organs and cause constriction of smooth muscle mediated by activation of phospholipase C—inositol-1,4,5-trisphosphate...
Adrenergic Receptors (Adrenoceptors): Classification01:27

Adrenergic Receptors (Adrenoceptors): Classification

Adrenergic receptors, or adrenoceptors, respond to the autonomic neurotransmitter noradrenaline and other endogenous catecholamine agonists. They are classified into two main families, α and β, based on their pharmacological response and are further subdivided depending on their location, elicited response, and affinity to specific agonists or antagonists.
α-Adrenoceptors
α-Adrenoceptors are classified into two main subtypes: α1 and α2. The α1 adrenoceptors, which are found on postsynaptic...
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...
Drugs Affecting Neurotransmitter Release or Uptake01:21

Drugs Affecting Neurotransmitter Release or Uptake

Certain drugs can affect how neurotransmitters called catecholamines, are released or taken back up in the adrenergic neuron. They can have different effects on the body's sympathetic transmission. Reserpine, a natural compound found in the Rauwolfia shrub, blocks a transporter called vesicular monoamine transporter (VMAT), which leads to a buildup of catecholamines in the cell and reduces sympathetic transmission. Another drug called guanethidine works in multiple ways, including blocking...

You might also read

Related Articles

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

Sort by
Same author

The association of frailty with age and lifespan in mice differs by strain and sex.

The journals of gerontology. Series A, Biological sciences and medical sciences·2026
Same author

High frailty index scores predict mortality and changes in blood-based biomarkers in aging female mice.

The journals of gerontology. Series A, Biological sciences and medical sciences·2026
Same author

Targeting Age-Associated Immune Senescence via Nanoparticle-Based Metabolic Reprogramming.

ACS nano·2026
Same author

Sodium nitrate supplementation prevents beneficial cardiac adaptations to running in female mice with few effects on male hearts.

Scientific reports·2026
Same author

Bedrest, frailty and exercise countermeasures: A 14-day head-down tilt study in mid-older aged adults.

Experimental gerontology·2026
Same author

Treatment with a selective androgen receptor modulator (RAD140) is linked to better cardiac function, with male-specific effects that are graded by interleukin-6.

GeroScience·2026

Related Experiment Video

Updated: Jun 28, 2026

Getting to Compliance in Forced Exercise in Rodents: A Critical Standard to Evaluate Exercise Impact in Aging-related Disorders and Disease
10:19

Getting to Compliance in Forced Exercise in Rodents: A Critical Standard to Evaluate Exercise Impact in Aging-related Disorders and Disease

Published on: August 22, 2014

The age-related decrease in catecholamine sensitivity is mediated by beta(1)-adrenergic receptors linked to a

Spring R Farrell1, Susan E Howlett

  • 1Department of Pharmacology, Dalhousie University, Halifax, Nova Scotia, Canada B3H 1X5.

Mechanisms of Ageing and Development
|November 1, 2008
PubMed
Summary
This summary is machine-generated.

Aging reduces catecholamine sensitivity in heart cells due to a defect in beta-1 adrenergic receptor (beta-AR) signaling, specifically impacting cyclic AMP (cAMP) production.

More Related Videos

Assessment of Vascular Tone Responsiveness using Isolated Mesenteric Arteries with a Focus on Modulation by Perivascular Adipose Tissues
08:41

Assessment of Vascular Tone Responsiveness using Isolated Mesenteric Arteries with a Focus on Modulation by Perivascular Adipose Tissues

Published on: June 3, 2019

Cardiac Stress Test Induced by Dobutamine and Monitored by Cardiac Catheterization in Mice
15:45

Cardiac Stress Test Induced by Dobutamine and Monitored by Cardiac Catheterization in Mice

Published on: February 10, 2013

Related Experiment Videos

Last Updated: Jun 28, 2026

Getting to Compliance in Forced Exercise in Rodents: A Critical Standard to Evaluate Exercise Impact in Aging-related Disorders and Disease
10:19

Getting to Compliance in Forced Exercise in Rodents: A Critical Standard to Evaluate Exercise Impact in Aging-related Disorders and Disease

Published on: August 22, 2014

Assessment of Vascular Tone Responsiveness using Isolated Mesenteric Arteries with a Focus on Modulation by Perivascular Adipose Tissues
08:41

Assessment of Vascular Tone Responsiveness using Isolated Mesenteric Arteries with a Focus on Modulation by Perivascular Adipose Tissues

Published on: June 3, 2019

Cardiac Stress Test Induced by Dobutamine and Monitored by Cardiac Catheterization in Mice
15:45

Cardiac Stress Test Induced by Dobutamine and Monitored by Cardiac Catheterization in Mice

Published on: February 10, 2013

Area of Science:

  • Cardiovascular Physiology
  • Cellular Aging
  • Adrenergic Signaling

Background:

  • Aging is associated with reduced responsiveness to catecholamines, crucial for regulating heart function.
  • The precise mechanisms underlying age-related deficits in beta-adrenergic receptor (beta-AR) signaling remain incompletely understood.

Purpose of the Study:

  • To investigate whether reduced catecholamine sensitivity in aged myocytes stems from defects in the beta-AR signaling pathway.
  • To elucidate the specific components of the beta-AR cascade affected by cellular aging.

Main Methods:

  • Simultaneous measurement of myocyte contractions and intracellular calcium (Ca2+) in ventricular myocytes from young and aged Fischer 344 rats.
  • Stimulation using beta(1)-AR and beta(2)-AR agonists, forskolin (adenylate cyclase activator), and phosphodiesterase inhibitors.
  • Direct measurement of cyclic adenosine monophosphate (cAMP) levels.

Main Results:

  • Aged myocytes required higher beta(1)-AR agonist concentrations for increased contraction, with similar Ca2+ transients compared to younger cells.
  • No age-related differences were observed with beta(2)-AR agonist stimulation.
  • Reduced cAMP production in aged myocytes upon beta-AR or adenylate cyclase stimulation, while downstream responses to dibutyryl cAMP were preserved.

Conclusions:

  • The age-related decline in catecholamine sensitivity is primarily mediated by beta(1)-ARs.
  • A defect in cAMP production downstream of beta(1)-AR activation contributes to impaired cardiac function in aged myocytes.
  • Post-cAMP signaling pathways remain largely unaffected by age.