Beta-adrenergic agonist

Beta adrenergic receptor agonists
Drug class

Albuterol

Skeletal structor formula of salbutamol (albuterol) — a widely used medication to treat asthma attacks
Class identifiers
Use Bradycardia, Asthma, heart failure, etc.
ATC code R03
Biological target Adrenergic receptors (β subtype)
External links
MeSH D000318

Beta adrenergic agonists or Beta agonists are medications that relax muscles of the airways, which widens the airways and results in easier breathing.[1] They are a class of sympathomimetic agents which act upon the beta adrenoceptors.[2] In general, pure beta-adrenergic agonists have the opposite function of beta blockers. Beta adrenoreceptor agonist ligands mimic the action of epinephrine and norepinephrine signaling in the heart, lungs and smooth muscle tissue, with epinephrine expressing the highest affinity. The activation of β1, β2 and β3 activates the enzyme, adenylate cyclase. This in turn leads to the activation of the secondary messenger cyclic adenosine monophosphate (cAMP), cAMP then activates Protein Kinase A (PKA) which phosphorylates target proteins ultimately inducing smooth muscle relaxation and contraction of the cardiac tissue.[3]

Function

Epinephrine (adrenaline)

Activation of β1 receptors induces positive inotropic, chronotropic output of the cardiac muscle, leading to increased heart rate and blood pressure, secretion of ghrelin from the stomach, and renin release from the kidneys.[4]

Activation of β2 receptors induces smooth muscle relaxation in the lungs, gastrointestinal tract, uterus, and various blood vessels. Increased heart rate and heart muscle contraction is also associated with the β2 receptors.

β3 receptors are mainly located in adipose tissue.[5] Activation of the β3 receptors induces the metabolism of lipids.[6]

Medical uses

Indications of administration for β agonists include the following:

Side effects

Although minor compared to those of epinephrine, beta agonists usually have mild to moderate adverse effects, which include anxiety, hypertension, increased heart rate and insomnia. Other side effects include headaches and essential tremor. Indications of hypoglycemia were also reported due to secretion of insulin in the body from activation of β2 receptors.

In 2013, zilpaterol, a β agonist sold by Merck was temporarily withdrawn due to signs of sickness in some cattle that were fed the drug.[7]

Receptor selectivity

Most agonists of the beta receptors are selective for one or more beta-adrenoreceptors. For example, patients with low heart rate are given beta agonist treatments that are more "cardio-selective" such as dobutamine, which increases the force of contraction of the heart muscle. Patients who are suffering from a chronic inflammatory lung diseases such as asthma or chronic obstructive pulmonary disease are treated with salbutamol (albuterol), which mainly induces smooth muscle relaxation in the lungs and less contraction of the heart.[8]

β3 agonists are currently in clinical research and are thought to increase the breakdown of lipids in obese patients.[9]

β1 agonists

β1 agonists: stimulates adenylyl cyclase activity; opening of calcium channel. (cardiac stimulants; used to treat cardiogenic shock, acute heart failure, bradyarrhythmias). Selected examples are:

β2 agonists

β2 agonists: stimulates adenylyl cyclase activity; closing of calcium channel (smooth muscle relaxants; used to treat asthma and COPD). Selected examples are:

Undetermined/unsorted

The following agents are also listed as agonists by MeSH.[10]

See also

References

  1. ↑ "WHAT ARE BETA-AGONISTS?". Thoracic.org. American Thoracic Society. Retrieved 17 October 2014.
  2. ↑ Adrenergic beta-Agonists at the US National Library of Medicine Medical Subject Headings (MeSH)
  3. ↑ Delbruck, Max. "The beta-adrenergic receptors".
  4. ↑ Yoo, B.; et al. "Beta1-adrenergic receptors stimulate cardiac contractility and CaMKII activation in vivo and enhance cardiac dysfunction following myocardial infarction".
  5. ↑ Johnson, M. "Molecular mechanisms of beta(2)-adrenergic receptor function, response, and regulation".
  6. ↑ Lowell, B.B.; Flier, J.S. (1997). "Brown adipose tissue, beta 3-adrenergic receptors, and obesity". Annu. Rev. Med. 48. pp. 307–16.
  7. ↑ "Archived copy". Archived from the original on 2013-08-27. Retrieved 2013-08-16.
  8. ↑ Pias, M.T. "The Pharmacology of Adrenergic Receptors".
  9. ↑ Meyers, D.S.; Skwish, S.; Dickinson, K.E.; Kienzle, B.; Arbeeny, C.M. (Feb 1997). "Beta 3-adrenergic receptor-mediated lipolysis and oxygen consumption in brown adipocytes from cynomolgus monkeys". J. Clin. Endocrinol. Metab. 82 (2). pp. 395–401.
  10. ↑ MeSH list of agents 82000318
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