Pharmacological properties of antidepressants

The pharmacological action of antidepressants is due to the following mechanisms: delayed recovery of norepinephrine, serotonin, and dopamine; sodium antagonistic effects; blockade of muscarinic acetylcholine receptors; histamine (HI) receptor block, alpha-1 receptor blockade, serotonin-2 (5-HT2) receptor blockade and dopamine Dopamine D2 receptor blockade (Kasper S., Moller H., Muller-Spahn F., 1997).

Antidepressants can mediate the intracellular signaling mechanisms that control neurotrophic processes, which ensures the functional viability of the neuronal systems of the brain.

Based antidepressant mechanism of action, are the following groups: selective serotonin reuptake inhibitors (fluoxetine, sertraline, paroxetine, fluvoxamine, citalopram), monoamine oxidase inhibitors (nialamide), reversible inhibitors of monoamine oxidase type A (pirazidol, moclobemide), selective blockers of noradrenaline reuptake ( mianserin, maprotiline), selective serotonin and noradrenalin reuptake inhibitors (venlafaxine, milnacipran), noradrenergic and serotonergic antidepressant (myrtle APIN), selective serotonin reuptake stimulator (tianeptine). Currently, there are drugs that selectively affect the exchange of the precursor of norepinephrine-dopamine (bupropion).

The pharmacological properties of antidepressants have a different effect on the clinical manifestations of depression. The blockade of norepinephrine reuptake by nerve endings leads to the reduction of depressive symptoms (psychomotor retardation, low mood), but at the same time it causes a number of side effects (tremor, tachycardia; dysfunction of men; arterial pressure lowering). The blockade of serotonin reuptake leads to the weakening of other manifestations of depression (anhedonia, circadian manifestations of depression, anxiety). The blockade of dopamine reuptake increases psychomotor activity, has antiparkinsonian effect, but at the same time can enhance the manifestations of psychosis. The blockade of histamine receptors enhances the effect of alcohol, barbiturates, neuroleptics, tranquilizers, leads to drowsiness, weight gain and hypotension. The blockade of muscarinic receptors (anticholinergic action) contributes to such side effects as blurred vision, dry mouth, tachycardia, constipation, urinary retention, memory impairment. The blockade of some adrenoreceptors leads to increased antihypertensive action of adrenergic blockers, orthostatic hypotension, dizziness, reflex tachycardia. Inhibition of type A monoamine oxidase (deamination of serotonin, norepinephrine, dopamine) has a stimulating effect (psychomotor activation, relief of depression), anxiety, insomnia, headache, neurotoxic disorders, the effect of sympathomimetic amines (adrenaline) may increase, and tyramine (neurotoxic) disorders, the effect of sympathomimetic amines (adrenaline) may develop, and tyramine (neurotoxic) disorders, the effect of sympathomimetic amines (adrenaline), and tyramine may increase (there may be neurotoxicity) “) Reaction. Inhibition of type B monoamine oxidase (deamination of phenylethylamine, benzylamine and dopamine) causes hemodynamic disorders, abnormal liver function, antiparkinsonian and antihypertensive effects.

Antidepressants are heterogeneous in terms of the effect on various manifestations of depression, in particular, on longing, apathy, anxiety, and motor stimulation. The nature of the effect on these components of depression underlies the clinical classification of antidepressants (Roose S. etal. 1994).

local_offerevent_note March 27, 2019

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