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Related Concept Videos

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...
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: 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.
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Heart Failure Drugs: β-Blockers01:22

Heart Failure Drugs: β-Blockers

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, vasodilation, and...
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Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
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Heart Failure II: Pathophysiology

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Implantation of an Isoproterenol Mini-Pump to Induce Heart Failure in Mice
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Beta 1-adrenergic receptor polymorphisms confer differential function and predisposition to heart failure.

Jeanne Mialet Perez1, Deborah A Rathz, Natalia N Petrashevskaya

  • 1Department of Medicine, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267, USA.

Nature Medicine
|September 23, 2003
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Summary

The Arg389 variant of beta(1)-adrenergic receptors (beta(1)-ARs) predisposes individuals to heart failure by altering signaling pathways. This genetic variation also impacts treatment response to beta-receptor blockers.

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Area of Science:

  • Cardiovascular biology
  • Pharmacogenetics
  • Molecular cardiology

Background:

  • Catecholamines enhance cardiac contractility via beta(1)-adrenergic receptors (beta(1)-ARs).
  • Human beta(1)-ARs exhibit polymorphism at amino acid residue 389, with Arg/Gly variants.
  • The Arg389 variant is associated with human heart failure phenotypes.

Purpose of the Study:

  • To investigate the mechanisms linking the Arg389 variant to heart failure.
  • To elucidate the functional consequences of the Arg389 variant in cardiac contractility and signaling.
  • To determine the influence of the Arg389 variant on therapeutic responses to beta-receptor blockade.

Main Methods:

  • Cardiac-targeted transgenesis in a mouse model.
  • Assessment of receptor function, adenylyl cyclase signaling, and cardiac contractility.
  • Analysis of gene expression, protein levels, and cardiac fibrosis.
  • Evaluation of hemodynamic responses and patient treatment outcomes.

Main Results:

  • Young Arg389 mice showed enhanced beta(1)-AR function and contractility compared to Gly389 mice.
  • Older Arg389 mice exhibited decreased beta-agonist signaling, reduced contractility, abnormal gene expression, and fibrosis.
  • Phenotypic changes in Arg389 mice mirrored those in failing human hearts.
  • Arg389 homozygosity correlated with improved ventricular function during carvedilol treatment.

Conclusions:

  • The human Arg389 variant predisposes to heart failure through hyperactive signaling, leading to receptor uncoupling and ventricular dysfunction.
  • This genetic variant influences the therapeutic efficacy of beta-receptor blockade in heart failure patients.