Drug acting on ANS

Adrenergic agonists and antagonists
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Defination and theory
Identify the structures of different drugs
Nomenclatures for different drugs
Physico-chemical properties, stability storage condition and different dosage forms


  • Information about drug used on ANS


Introduction to Adrenergic agonists and antagonists

An adrenergic agonist is a drug that stimulates a response from the adrenergic receptors. The five main categories of adrenergic receptors are: α1, α2, β1, β2, and β3, although there are more subtypes, and agonists vary in specificity between these receptors, and may be classified respectively. However, there are also other mechanisms of adrenergic agonism. Epinephrine and norepinephrine are endogenous and broad-spectrum. More selective agonists are more useful in pharmacology.

An adrenergic antagonist is a drug that inhibits the function of adrenergic receptors. There are five adrenergic receptors, which are divided into two groups. The first group of receptors are the beta (β) adrenergic receptors. There are β1, β2, and β3 receptors. The second group contains the alpha (α) adrenoreceptors. There are only α1 and α2 receptors. Adrenergic receptors are located near the heart, kidneys, lungs, and gastrointestinal tract.[1] There are also α-adreno receptors that are located on vascular smooth muscle.[2]

Antagonists reduce or block the signals of agonists. They can be drugs, which are added to the body for therapeutic reasons, or endogenous ligands. The α-adrenergic antagonists have different effects from the β-adrenergic antagonists.

An adrenergic agent is a drug, or other substance, which has effects similar to, or the same as, epinephrine (adrenaline). Thus, it is a kind of sympathomimetic agent. Alternatively, it may refer to something which is susceptible to epinephrine, or similar substances, such as a biological receptor (specifically, the adrenergic receptors).

Adrenergic ligands are endogenous proteins that modulate and evoke specific cardiovascular effects. Adrenergic antagonists reverse the natural cardiovascular effect, based on the type of adrenoreceptor being blocked. For example, if the natural activation of the α1-adrenergic receptor leads to vasoconstriction, an α1-adrenergic antagonist will result in vasodilation.

Some adrenergic antagonists, mostly β antagonists, passively diffuse from the gastrointestinal tract. From there, they bind to albumin and α1-acid glycoprotein in the plasma, allowing for a wide spread through the body. From there, the lipophilic antagonists are metabolized in the liver and eliminated with urine while the hydrophilic ones are eliminated unchanged.

Directly acting adrenergic agonists act on adrenergic receptors. All adrenergic receptors are G-protein coupled, activating signal transduction pathways. The G-protein receptor can affect the function of adenylate cyclase or phospholipase C, an agonist of the receptor will upregulate the effects on the downstream pathway (it will not necessarily upregulate the pathway itself).

The receptors are broadly grouped into α and β receptors. There are two subclasses of α-receptor, α1 and α2 which are further subdivided into α1A, α1B, α1D, α2A, α2B and α2C. The α2C receptor has been reclassed from α1C, due to its greater homology with the α2 class, giving rise to the somewhat confusing nomenclature. The β receptors are divided into β1, β2 and β3. The receptors are classed physiologically, though pharmacological selectivity for receptor subtypes exists and is important in the clinical application of adrenergic agonists (and, indeed, antagonists).

From an overall perspective, α1 receptors activate phospholipase C (via Gq), increasing the activity of protein kinase C (PKC); α2 receptors inhibit adenylate cyclase (via Gi), decreasing the activity of protein kinase A (PKA); β receptors activate adenylate cyclase (via Gs), thus increasing the activity of PKA. Agonists of each class of receptor elicit these downstream responses.

Indirectly acting adrenergic agonists affect the uptake and storage mechanisms involved in adrenergic signalling.

Two uptake mechanisms exist for terminating the action of adrenergic catecholamines - uptake 1 and uptake 2. Uptake 1 occurs at the presynaptic nerve terminal to remove the neurotransmitter from the synapse. Uptake 2 occurs at postsynaptic and peripheral cells to prevent the neurotransmitter from diffusing laterally.

There is also enzymatic degradation of the catecholamines by two main enzymes - monoamine oxidase and catechol-o-methyl transferase. Respectively, these enzymes oxidise monoamines (including catecholamines) and methylate the hydroxal groups of the phenyl moiety of catecholamines. These enzymes can be targeted pharmacologically. Inhibitors of these enzymes act as indirect agonists of adrenergic receptors as they prolong the action of catecholamines at the receptors.

A great number of drugs are available which can affect adrenergic receptors. Other drugs affect the uptake and storage mechanisms of adrenergic catecholamines, prolonging their action. The following headings provide some useful examples to illustrate the various ways in which drugs can enhance the effects of adrenergic receptors.

While only a few α-adrenergic antagonists are competitive, all β-adrenergic antagonists are competitive antagonists. Competitive antagonists are a type of reversible antagonists. A competitive antagonist will attach itself to the same binding site of the receptor that the agonist will bind to. Even though it is in activator region, the antagonist will not activate the receptor. This type of binding is reversible as increasing the concentration of agonist will outcompete the concentration of antagonist, resulting in receptor activation.

Adrenergic competitive antagonists are shorter lasting than the other two types of antagonists. While the antagonists for alpha and beta receptors are usually different compounds, there has been recent drug development that effects both types of the adrenoreceptors.

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Urmila Gavali
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Myself Mrs. Urmila Ravindra Gavali, Completed B. Pharm and M. Pharm in Quality assurance techniques from PREs College of Pharmacy, chincholi. Currently worked as Lecturer in K. K. Wagh Institute of Pharmacy, Nashik.

I had published research paper in WJPR on the topic of

i) Phytochemical constituents present in wheatgrass powder and wheatgrass juice.

ii) Combinatorial chemistry: A new drug approach for Drug Design.

I had Published review article in WJPR on the topic of Covid 19: A review.

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