## Analysis of Alpha-Blocker Selectivity and Cardiovascular Effects **Key Point:** Prazosin is a selective α1-blocker, but selectivity for α1A vs. α1B receptors does NOT explain differences in tachycardia. All selective α1-blockers (prazosin, doxazosin, terazosin) cause similar reflex tachycardia because they block α1-receptors on vascular smooth muscle, leading to vasodilation and baroreceptor-mediated sympathetic activation. ### Correct Answer Explanation The statement about prazosin causing less tachycardia due to α1A selectivity is **incorrect**. Prazosin does cause less tachycardia than doxazosin, but the reason is **pharmacokinetic** (rapid absorption and peak levels), not receptor selectivity. Both drugs are non-selective α1-blockers; the α1A/α1B distinction does not explain the tachycardia difference. ### Why the Other Statements Are Correct | Agent | Property | Evidence | |-------|----------|----------| | Terazosin | Longer half-life (12–13 hrs) | Can be dosed once daily; longer than prazosin (2–3 hrs) | | Phenoxybenzamine | Non-selective, irreversible | Covalent binding; used for preoperative pheochromocytoma prep | | Alfuzosin | α1A-selective | Improved LUTS symptom relief in BPH; lower incidence of syncope | **Clinical Pearl:** The first-dose syncope seen with prazosin is due to rapid peak levels causing acute vasodilation, not α1A selectivity. Slow titration and bedtime dosing mitigate this risk. **High-Yield:** α1A receptors predominate in the prostate and bladder neck; α1B receptors are in vascular smooth muscle. Newer agents (alfuzosin, silodosin) target α1A to improve BPH symptoms while reducing vasodilation.
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