Related Experiment Video

Updated: Aug 3, 2026

In Vitro Assays to Evaluate the Migration, Invasion, and Proliferation of Immortalized Human First-trimester Trophoblast Cell Lines
09:57

In Vitro Assays to Evaluate the Migration, Invasion, and Proliferation of Immortalized Human First-trimester Trophoblast Cell Lines

Published on: March 5, 2019

Inhibition of beta-adrenergic responsiveness in muscle cell cultures by dexamethasone

T J Smith, R Dana, A Krichevsky

    Endocrinology
    |December 1, 1981
    PubMed

    Insights

    Dexamethasone, a glucocorticoid, inhibits muscle cell development (myogenesis) and reduces beta-adrenergic responsiveness in cell cultures. These effects are dose-dependent, impacting cell function and receptor levels.

    Area of Science:

    • Biochemistry
    • Cell Biology
    • Pharmacology

    Background:

    • Myogenesis is the process of skeletal muscle formation.
    • Beta-adrenergic signaling plays a role in muscle cell function.
    • Glucocorticoids are steroid hormones with diverse physiological effects.

    Purpose of the Study:

    • To investigate the effects of dexamethasone on myogenic cell lines.
    • To determine if dexamethasone impacts beta-adrenergic responsiveness.
    • To explore the relationship between glucocorticoids, myogenesis, and adrenergic signaling.

    Main Methods:

    • Culturing L6E9 and L8 myogenic cell lines.
    • Treating cells with varying concentrations of dexamethasone.
    • Measuring adenylate cyclase activity and cAMP accumulation.
    • Assessing beta-adrenergic receptor density using radioligand binding.

    Main Results:

    • Dexamethasone completely inhibited myotube formation at 1 microM and partially inhibited it at 1 nM.
    • Beta-adrenergic responsiveness, including isoproterenol-stimulated adenylate cyclase activity and cAMP levels, was decreased by dexamethasone.
    • The number of beta-adrenergic receptors decreased in parallel with cAMP levels in the presence of dexamethasone.
    • A high-affinity cytosolic binding site for triamcinolone acetonide increased with developmental state.

    Conclusions:

    • Glucocorticoids, such as dexamethasone, inhibit myogenesis in vitro.
    • Dexamethasone impairs beta-adrenergic responsiveness in myogenic cells.
    • These findings suggest a significant role for glucocorticoids in regulating muscle development and function.

    More Related Videos

    Primary Culture of Rat Adrenocortical Cells and Assays of Steroidogenic Functions04:33

    Primary Culture of Rat Adrenocortical Cells and Assays of Steroidogenic Functions

    Published on: March 12, 2019

    Preclinical Drug Testing in Scalable 3D Engineered Muscle Tissues08:07

    Preclinical Drug Testing in Scalable 3D Engineered Muscle Tissues

    Published on: April 7, 2023

    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 Antagonists: Chemistry and Classification of β-Receptor Blockers01:25

    Adrenergic Antagonists: Chemistry and Classification of β-Receptor Blockers

    β-adrenergic antagonists, or β-blockers, modulate the sympathetic nervous system by targeting β-adrenoceptors and inhibiting catecholamine-mediated sympathetic responses. β-blockers differ in their adrenoceptor subtype affinity, lipophilicity, and α-blocking capabilities. The history of β-blocker development began with the prototype, dichloroisoprenaline, which exhibited partial agonist activity. As a result, propranolol was developed as a pure antagonist but nonselective agent, paving the way...
    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...
    Adrenergic Antagonists: ɑ and β-Receptor Blockers01:31

    Adrenergic Antagonists: ɑ and β-Receptor Blockers

    Third-generation β-blockers, such as labetalol and carvedilol, represent a significant advancement in managing cardiovascular conditions. Unlike conventional β-blockers, which can induce peripheral vasoconstriction, third-generation drugs block α1 adrenoceptors. This promotes vasodilation through several mechanisms, such as increased nitric oxide production, inhibition of calcium ion entry, opening of potassium ion channels, and antioxidant action. Labetalol, for instance, is clinically...
    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...
    Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers01:24

    Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers

    Adrenergic stimulation generally impacts cardiac rate and rhythm. Specifically, stimulation of the β-adrenoceptors triggers an increase in intracellular calcium ion influx and pacemaker currents, which may cause arrhythmias. Catecholamines like adrenaline also demonstrate β2-adrenoceptor-mediated hypokalemia, impacting cardiac action potential and disrupting the normal cardiac rhythm. Class II antiarrhythmic drugs are β-adrenoceptor antagonists or β-blockers, which indirectly block calcium...