Levodopa :
It is actively transported into the CNS and is converted to dopamine in the brain. This leads to replenishment of dopamine in the brain.
Carpidopa :
It diminishes the metabolism of levodopa in the GIT and peripheral tissues ,thereby increasing the availability of levodopa in the CNS .
Selegiline :
It inhibits MAO type B that metabolizes dopamine. This increase dopamine levels in the brain and enhance levodopa action.
Entacapone :
It selectively and reversibly inhibits COMT . This leads to decreased plasma concentration of 3-O-methyldopa , increased central uptake of levodopa and greater concentrations of brain dopamine.
Memantine :
It physically block the NMDA receptor-associated ion channels . This slow the rate of memory loss in Alzheimer disease.
Mitoxantrone :
It modifies the body's immune response through inhibition of inflammatory processes mediated by white blood cells that eventually lead to myelin sheath damage and decreased axonal communication between cells.
Fingolimod :
It alters lymphocyte migration resulting in sequestration of lymphocytes in lymph nodes.
Benzodiazepines :
It binds to a specific high affinity site located at the interface of the α subunit and γ2 subunit of GABA receptor. This leads to increased frequency of Cl channels opening and greater entry of chloride ions which hyper-polarizes the cell making it more difficult to depolarize and reduces neural excitability.
Buspirone :
It is a partial agonist for serotonin receptors , it blocks these receptors and reduce neural excitability . ( Useful for chronic treatment of GAD )
Barbiturates:
It binds to a specific site on GABA receptors and prolong duration of Cl channels opening so enhance GABA-ergic transmission.
Disulfiram :
It blocks the oxidation of acetaldehyde to acetic acid by inhibiting aldehyde dehydrogenase. This results in accumulation of acetaldehyde in the blood leading to unpleasant effects and the patient abstains from alcohol drinking.
Methylxanthines ( Theophylline , Tea ) :
It increases cAMP and cGMP by inhibiting phosphodiestrase enzyme.
** Other proposed mechanisms include : blockade of adenosine receptors and
translocation of Ca extracellular.
Inhaled Anesthetics :
( The EXACT mechanism is unknown )
It increases the sensitivity of GABA receptors to GABA > prolongation of the inhibitory chloride ion current > diminished neuronal excitability.
Local Anesthetics ( Amides and Esters ) :
( Bubivacaine , Lidocaine , Mepivacaine ... )
It blocks sodium channels to prevent the transient increase in permeability of membrane to sodium that is required for action potential to occur . This leads to blockade of nerve conduction of sensory impulses from the periphery to the CNS.
Anti-psychotics ( 1st Generation ) :
( Chlorpromazine , prochlorperazin ..... )
Competitive inhibitors at variety of receptors especially D2 dopamine receptors in the brain and periphery.
Anti-psychotics ( 2nd Generation ) :
( Aripiprazole , Asenapine , Risperidone .... )
Competitive inhibitors of dopamine receptors in the brain and periphery and inhibition of serotonin receptors.
Opioids :
( Morphine , Meperidine , Methadone .....)
It binds to opioid receptors in the CNS and other autonomic structures , This causes hyperpolarization of nerve cells , inhibition of nerve firing and presynaptic inhibition of transmitter release. This leads to decrease in painful stimuli and relieve of intense pain.
Anti-epileptics :
( Carbamazepine , Ethosuximide .... )
1- Blocking voltage-gated channels ( Na or Ca ).
2- Enhancing inhibitory GABA-ergic impulses.
3- Interfering with excitatory glutamate transmission.
Valproic acid ( Valproate ) :
1- Sodium channel blockade
2- Blockade of GABA transaminase
3- Action on the T type calcium channels
NEXT PART : MECHANISM OF ACTION FOR ALL DRUGS ACTING ON CVS.
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