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Adrenergic Receptors: ɑ Subtype

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 Subtype

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 Receptors (Adrenoceptors): Classification

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...

GPCRs Regulate Adenylyl Cylase Activity

GPCRs Regulate Adenylyl Cylase Activity

Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of cells.
Two...

Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers

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...

Adrenergic Antagonists: Pharmacological Actions of ɑ-Receptor Blockers

Adrenergic Antagonists: Pharmacological Actions of ɑ-Receptor Blockers

α-Adrenergic antagonists, known as α-blockers, exert their effects by inhibiting α-adrenoceptors, leading to specific physiological actions. α1-blockers and α2-blockers have distinct pharmacological actions and therapeutic applications.
α1-blockers: These drugs inhibit α1-adrenoceptors on smooth muscle cells, resulting in vasodilation. This vasodilation lowers blood pressure, making α1-blockers valuable in treating hypertension. Additionally, α1-blockers effectively address urinary obstruction...

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Related Experiment Video

Updated: Jun 6, 2026

Drug-induced Sensitization of Adenylyl Cyclase: Assay Streamlining and Miniaturization for Small Molecule and siRNA Screening Applications

Drug-induced Sensitization of Adenylyl Cyclase: Assay Streamlining and Miniaturization for Small Molecule and siRNA Screening Applications

Published on: January 27, 2014

Modulating proton sensing by the adenosine receptor A2.

Kyutae D Lee, Sam Taylor, Daniel G Isom

Biorxiv : the Preprint Server for Biology

|June 5, 2026

Summary

Researchers discovered novel mechanisms for how G-protein-coupled receptors (GPCRs) sense pH. A specific mutation in adenosine A2A receptors (A2AR) eliminated pH sensitivity, offering new insights into receptor function.

Area of Science:

Biochemistry
Molecular Biology
Pharmacology

Background:

G-protein-coupled receptors (GPCRs) traditionally thought to sense pH via external histidine residues.
Recent findings indicate internal acidic amino acids in known acid-sensing GPCRs (GPR4, GPR65, GPR68).
Adenosine A2A receptor (A2AR) activation at low pH occurs without the typical acidic triad structure.

Purpose of the Study:

Investigate the proton-sensing mechanism of the adenosine A2A receptor (A2AR).
Identify structural components responsible for pH sensitivity in A2AR.
Explore novel pH-sensing mechanisms in GPCRs.

Main Methods:

Utilized bioinformatics analysis.
Employed a humanized yeast-based platform (DCyFIR) for screening.

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Methods for the Discovery of Novel Compounds Modulating a Gamma-Aminobutyric Acid Receptor Type A Neurotransmission

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Drug-induced Sensitization of Adenylyl Cyclase: Assay Streamlining and Miniaturization for Small Molecule and siRNA Screening Applications

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Methods for the Discovery of Novel Compounds Modulating a Gamma-Aminobutyric Acid Receptor Type A Neurotransmission

Methods for the Discovery of Novel Compounds Modulating a Gamma-Aminobutyric Acid Receptor Type A Neurotransmission

Published on: August 16, 2018

Validated findings in mammalian cells.

Main Results:

Identified mutations that abolish A2AR pH sensitivity while maintaining agonist signaling.
Demonstrated that the N284D mutation eliminates pH sensing and enhances agonist potency.
Provided a novel structural model for pH sensing and sodium binding in A2AR.

Conclusions:

GPCRs exhibit diverse pH-sensing mechanisms beyond established models.
The study reveals a novel, pH-insensitive A2AR variant with potential applications.
Findings challenge previous assumptions about GPCR pH modulation.