β-Blocker Selectivity Nonselective β-Antagonists (β1 = β2) Drug Effect Clinical Applications Toxicity Propranolol, nadolol, timolol Lowers BP and HR Reduces renin secretion Decreases cardiac ouptut and increases peripheral resistance Hypertension Arrhythmias Angina pectoris Migraines Hyperthyroidism Glaucoma (timolol) Bradycardia Fatigue Worsening asthma Vivid dreams β1-Selective Antagonist (β1 > β2) Drug Effect Clinical Applications Toxicity Metoprolol, atenolol, betaxolol Lowers BP and HR Reduces renin secretion Hypertension Arrhythmias Angina pectoris Same toxicity as nonselective ß-antagonists but safer in asthma Esmolol Very rapid onset of action (10 min half-life) Rapid control of supraventricular arrhythmias, BP, and thyrotoxicosis Bradycardia Hypotension Nonselective α- and β-Antagonists (β1 = β2≥ α1 > α2) Drug Effect Clinical Applications Toxicity Labetalol, carvedilol Heart failure Fatigue Partial β-Agonists (β1 = β2 Blockade with Some β-Agonist Activity) Drug Effect Clinical Applications Toxicity Acebutolol, pindolol, carteolol Lowers HR less than the effect on BP Hypertension Arrhythmias Hypotension but less tachycardia than alpha blockers such as phentolamine Mechanism of Action for Clinical Application Mechanism of Action for Clinical Application Clinical Application Mechanism Hypertension ↓ Cardiac output ↓ Renin secretion by blocking β-receptor on JGA cells Angina pectoris ↓ O2 consumption by ↓ heart rate and contractility SVT (propranolol, esmolol) ↓ AV conduction velocity MI ↓ Mortality CHF Slows progression Glaucoma (timolol) ↓ Secretion of aqueous humor