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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 β 1, β 2, and β 3 receptors. The second group contains the alpha (α) adrenoreceptors.
Noradrenergic and specific serotonergic antidepressants (NaSSAs) are a class of psychiatric drugs used primarily as antidepressants. [1] They act by antagonizing the α 2 -adrenergic receptor and certain serotonin receptors such as 5-HT 2A and 5-HT 2C , [ 1 ] but also 5-HT 3 , [ 1 ] 5-HT 6 , and/or 5-HT 7 in some cases.
Antiadrenergic agents inhibit the signals of epinephrine and norepinephrine. They are primarily postsynaptic adrenergic receptor antagonists (alpha and beta adrenergic receptor antagonists, or "blockers"), inhibiting the downstream cellular signaling pathways of adrenergic receptors .
Specific locations and functions of the α receptors. Image from Basic and Clinical Pharmacology by Bertram Katzung, et al. [1] Alpha blockers, also known as α-blockers or α-adrenoreceptor antagonists, are a class of pharmacological agents that act as antagonists on α-adrenergic receptors (α-adrenoceptors).
The mechanisms of sympathomimetic drugs can be direct-acting (direct interaction between drug and receptor), such as α-adrenergic agonists, β-adrenergic agonists, and dopaminergic agonists; or indirect-acting (interaction not between drug and receptor), such as MAOIs, COMT inhibitors, release stimulants, and reuptake inhibitors that increase the levels of endogenous catecholamines.
Adrenergic blocking agents are a class of drugs that exhibit its pharmacological action through inhibiting the action of the sympathetic nervous system [1] in the body. The sympathetic nervous system(SNS) is an autonomic nervous system that we cannot control by will.
The pharmacology of antidepressants is not entirely clear.. The earliest and probably most widely accepted scientific theory of antidepressant action is the monoamine hypothesis (which can be traced back to the 1950s), which states that depression is due to an imbalance (most often a deficiency) of the monoamine neurotransmitters (namely serotonin, norepinephrine and dopamine). [1]
Higher selectivity is associated with less off-target binding, which is binding between drug molecules and receptors other than target receptors. [6] Therefore, non-selective adrenergic blockers can cause various adverse effects as they can also exert actions on non-target receptors, such as non-selective alpha blockers and beta blockers. [6]