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Related Concept Videos

Adrenergic Antagonists: Pharmacological Actions of β-Receptor Blockers01:27

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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...
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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...
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β-adrenergic antagonists, commonly known as β-blockers, block the effects of sympathetic neurotransmitters such as noradrenaline (NA) and adrenaline (ADR). They have several beneficial effects in heart failure treatment. They reduce heart rate, the force of contraction, and cardiac muscle relaxation. They also slow the atrial-ventricular conduction rate and raise the threshold for arrhythmias. The concentration of β-blockers determines their effects on bronchodilation,...
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Adrenergic Antagonists: ɑ and β-Receptor Blockers01:31

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

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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...
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Antihypertensive Drugs: Action of β1 Blockers01:17

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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,...
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Spatial and Temporal Control of Murine Melanoma Initiation from Mutant Melanocyte Stem Cells
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Beta Blockers and Melanoma.

Aleksandra Vojvodic1, Petar Vojvodic2, Tatjana Vlaskovic-Jovicevic2

  • 1Department of Dermatology and Venereology, Military Medical Academy, Belgrade, Serbia.

Open Access Macedonian Journal of Medical Sciences
|December 19, 2019
PubMed
Summary
This summary is machine-generated.

Beta-blockers show promise in treating melanoma by inhibiting tumor growth and improving patient prognosis. They target tumor angiogenesis and immune suppression, offering potential as an adjuvant therapy.

Keywords:
Beta-blockersMelanoma

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Area of Science:

  • Oncology
  • Immunology
  • Pharmacology

Background:

  • Cancer immune-tolerance presents a significant challenge in oncology.
  • Beta-blockers exhibit potential anticarcinogenic effects across various cancers, including melanoma.
  • However, beta-blockers can also cause or exacerbate dermatological conditions.

Purpose of the Study:

  • To investigate the mechanisms behind the anticarcinogenic effects of beta-blockers in melanoma.
  • To explore the role of specific adrenoceptors in melanoma progression and immune response.
  • To evaluate the therapeutic potential of beta-blockers as an adjuvant therapy for melanoma.

Main Methods:

  • Analysis of beta-blocker effects on melanoma cell proliferation, angiogenesis, and invasiveness.
  • Investigation of adrenoceptor expression (β2 and β3) in immune cells under hypoxic conditions.
  • Assessment of changes in immune cell populations (Treg, MDSC, NK, CD8) and their cytotoxicity.

Main Results:

  • Beta-blockers, particularly propranolol, significantly improve melanoma patient prognosis.
  • Propranolol inhibits melanoma by reducing tumor angiogenesis, proliferation, and invasiveness, while mitigating local immune suppression.
  • Hypoxia upregulates β3-adrenoceptors in peripheral blood mononuclear cells, specifically in immune cells like Treg, MDSC, and NK cells, enhancing NK and CD8 cell number and cytotoxicity.

Conclusions:

  • Catecholamines may impede melanoma progression.
  • Beta-blockers possess unrecognized therapeutic potential for melanoma prevention and treatment.
  • Beta-blockers can serve as an effective adjuvant therapy alongside other melanoma treatments.