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Many tricyclic antidepressants, tetracyclic antidepressants, antipsychotics, ergolines, and some piperazines like buspirone, trazodone, nefazodone, etoperidone, and mepiprazole antagonize α 1-adrenergic receptors as well, which contributes to their side effects such as orthostatic hypotension.
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.
Mirtazapine, sold under the brand name Remeron among others, is an atypical tetracyclic antidepressant, and as such is used primarily to treat depression. [11] [12] Its effects may take up to four weeks but can also manifest as early as one to two weeks.
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.
They are mainly used in research, having found limited clinical application in human medicine. They are extensively used in veterinary medicine to reverse the effects of alpha-2 agonist drugs used as sedatives, like xylazine, medetomidine and dexmedetomidine. Alpha-2 blockers increase noradrenaline release.
Medications such as clonidine and dexmedetomidine target pre-synaptic auto receptors, therefore leading to an overall decrease in norepinephrine which clinically can cause effects such as sedation, analgesia, lowering of blood pressure and bradycardia. There is also low quality evidence that they can reduce shivering post operatively.
Midodrine is a prodrug which forms the active metabolite, desglymidodrine, which is an α 1-adrenergic receptor agonist and exerts its actions via activation of α 1-adrenergic receptors of the arteriolar and venous vasculature, producing an increase in vascular tone and elevation of blood pressure.
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]