Nortriptyline is a tricyclic antidepressant of the dibenzocycloheptene type and is the active metabolite of amitriptyline. Nortriptyline is similar to protriptyline. Medications in this class are often referred to as tricyclic antidepressants, or TCAs. Depression is an all-pervasive sense of sadness and gloom. In some patients with depression, abnormal levels of brain neurotransmitters (chemicals that the nerve cells use to communicate with each other) may be responsible for the depression. Nortriptyline elevates the mood ("anti-depresses") by raising the level of neurotransmitters in brain tissue.
Nortriptyline is used to elevate the mood of patients with depression. Nortriptyline is also a sedative and is useful in depressed patients with insomnia, restlessness, and nervousness. It also has been found to be helpful for treating chronic pain and the pain of neuralgia. Nortriptyline is used to relieve symptoms of depression such as feelings of sadness, worthlessness, or guilt; loss of interest in daily activities; changes in appetite; tiredness; sleeping too much; insomnia; and thoughts of death or suicide
It is believed that the most important effect is the enhancement of the actions of norepinephrine and serotonin caused by blocking the reuptake of various neurotransmitters at the neuronal membrane. Nortriptyline is more likely to inhibit the reuptake of serotonin than norepinephrine. There is more likelihood of orthostatic hypotension occurring with nortriptyline than with other tricyclics. Recent evidence suggests that the upset of monoamine output seen in depressed patients may be regulated by antidepressants following long-term treatment due to their action on œ-adrenergic receptors. This action on œ-receptors may be a better explanation than the reuptake theory for their antidepressant effects. Monoamine oxidase is not inhibited by nortriptyline. Tricyclic antidepressants do not affect dopamine reuptake. Varying degrees of sedation can be produced and is low to moderate for nortriptyline, and the seizure threshold can be lowered. Anticholinergic activity is strong and may be responsible for the inhibition of urination in the treatment of enuresis. Cardiac dysrhythmias may result from the direct quinidine-like effect on cardiac function in combination with anticholinergic activity and the potentiation of norepinephrine. Changes in sex hormone concentrations and blood glucose may result from the effect of nortriptyline on the endocrine system.