Prazosin administered to a patient with BPH causes postural hypotension. Which mechanism best explains the hypotension, distinct from its therapeutic effect on the bladder outlet?

• A Blockade of presynaptic alpha-2 receptors enhances norepinephrine release
• B Blockade of postsynaptic alpha-1 receptors on vascular smooth muscle causes vasodilation ✓
• C Partial agonism at alpha-2 receptors reduces sympathetic tone centrally
• D Inverse agonism at beta-1 receptors reduces cardiac output

Explanation

Prazosin selectively blocks postsynaptic alpha-1 adrenergic receptors on arteriolar and venous smooth muscle, reducing peripheral vascular resistance and causing vasodilation. The hypotension is predominantly postural because venodilatation impairs venous return. Because prazosin spares presynaptic alpha-2 receptors, it does not markedly increase reflex norepinephrine release—a key advantage over non-selective alpha-blockers. Its benefit in BPH is via blockade of alpha-1 receptors in the internal urethral sphincter and prostate capsule.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.