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Prazosin

Unchecked
From Pharmacopedia
Alpha-1 Adrenergic Antagonist
Prazosin
Minipress
Prazosin is best known in psychiatry as an off-label treatment for PTSD nightmares, it suppresses noradrenergic hyperactivity at night and reduces both nightmare frequency and severity in many patients. Originally an antihypertensive; now more often prescribed in mental health than cardiology. First-dose orthostatic hypotension is well-known, start at 1 mg HS and titrate slowly.

Experience

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Problems

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Titration strategies

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Effects

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Pharmacokinetics

Absorption

~60% oral bioavailability.

Distribution

Plasma protein binding ~97%.

Metabolism

Extensive hepatic metabolism.

Elimination

Primarily fecal as metabolites.

Interactions

Pharmacogenomic + mechanism interactions2 edges
Pharmacokinetic mechanismSubstrate / metabolism relationships from primary literature
Transporter:ABCG2 substrate Primary 70 / 100
FDA Drug Interactions Table: transporter substrate (ABCG2).
Inferred from pharmacokinetic dataMaterialised by the inference engine; provenance shown per row
Novobiocin pk raises via ABCG2 Inferred 49 / 100
Novobiocin inhibits ABCG2 (inhibitor, intensity 70); Prazosin is a substrate of ABCG2 (intensity 70). Derived: Prazosin exposure raised.
Inferred via Enzyme:ABCG2 (exposure raised)

Patient experience

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Monitoring

Blood pressure (especially orthostatic) during titration.

Patient counseling

First-dose effect: marked orthostatic hypotension within 30–90 min. Take initial dose at bedtime. Rise slowly from supine. Effect on nightmares emerges in 1–3 weeks; titrate by 1–2 mg every few nights as needed.

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Relevant Literature

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See also

Clonidine, Guanfacine

References

Summary
Classes
Alpha-1 Adrenergic Antagonist
Common uses
PTSD nightmares0, Hypertension0, BPH0
Pharmacy
Starting dose
1 mg at bedtime (PTSD nightmares); 1 mg BID–TID (HTN)
Preparations
1, 2, 5 mg caps
US FDA Max
40 mg/d
Pharmacology
Routes
Oral
Onset
30–90 min
Duration
6–8 h
Half-life
2–3 h
Bioavailability
~60%
Pregnancy
Category C
Legal status
Rx-only in US
Purported mechanism
Selective alpha-1 adrenergic receptor antagonist. Lowers peripheral vascular resistance via vasodilation; in the CNS, blunts noradrenergic hyperarousal thought to drive trauma-related nightmares.