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Mechanism of Action
  • Amphetamines cause release of stored norepinephrine from adrenergic neuron nerve terminals into the synaptic cleft. They appear to do so through a variety of distinct mechanisms. In this way, adrenergic receptors are stimulated but by an "indirect" mechanism as amphetamines do not directly bind these receptors (hence they are termed "Indirect Adrenergic Agonists").
Pharmacological Effects
  • Overview
    • Although the therapeutic and abuse potential of amphetamines lies in their central effects, peripheral adrenergic neurons of the sympathetic nervous system are also affected. Indeed, these autonomic effects are make up some of the important adverse and dose-limiting toxicities of these drugs.
  • Central Effects
    • Amphetamines are potent central-acting drugs that increase wakefulness, alertness, decrease fatigue, and reduce appetite. The adverse effects of these drugs are extensions of the previous and include insomnia, anorexia, tremor, irritability, and headache. At toxic doses seizures may occur.
  • Cardiovascular Effects
    • The primary autonomic effects of amphetamines are on the vasculature and heart. Activation of alpha1 receptors can lead to significant vasoconstriction while at higher doses activation of beta1 receptors can increased heart rate and contractility. Together these effects can yield prominent systolic and diastolic hypertension. At toxic doses individuals may feel palpitations that can ultimately evolve into frank arrhythmias.
Individual Compounds
  • Methylphenidate
  • Dextroamphetamine