Nebivolol, a third-generation beta-blocker, lowers blood pressure through an additional mechanism not shared by propranolol. This additional mechanism is:
- A Activation of alpha-1 receptors causing vasoconstriction
- B Calcium channel blockade in vascular smooth muscle
- C Potassium channel opening causing hyperpolarization
- D Endothelium-dependent vasodilation through increased nitric oxide (NO) bioavailability ✓
Explanation
Nebivolol is a highly selective beta-1 blocker that uniquely promotes endothelial nitric oxide synthase (eNOS) activation via the L-arginine–NO pathway, causing vasodilation — an effect mediated through beta-3 receptor stimulation on endothelial cells. This NO-mediated vasodilation lowers peripheral resistance in addition to the beta-1 blockade effect, resulting in better tolerability and possibly fewer metabolic adverse effects than older beta-blockers.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
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Written and medically reviewed by the StethoPrep medical team.