B-Adrenoceptor Antagonist

Ishemic Heart Disease

• reduce angina attacks
• improves excercise tolerance
• dec work load
• strongly indicated for use in acute phase of myocardial ischemia

• little effect in healthy subjects
• blockade of B2 adrenoceptors in bronchii can cause life threatening bronchoconstriction in patients with asthma or COPD

• reduced glycogenolysis and mobilization of glucose in response to hypoglycemia
• reduced activation of lipases and dec release of free fatty acids

effects on the eye:

• reduced intraocular pressure for glaucoma

• 1st gen Non -selective
• equal affinity B1=B2
• t1/2 - 3-6 hrs
• high lipophilic - oral admin
• metabol. in liver - first pass effect
• some mild CNS effects (sedation & dec libido)
• reduces HR and BP
• uses: hypertension, angina, arrythmias, MI, CHF

• t1/2 - 4-5 hrs
• less lipid soluble
• no local anesthetic effects
• therapeutic uses: hypertension, angina migrane, open angle glaucoma

• t1/2 - 3-4 hrs
• partial agonist activity at B1 & B2 receptors
• less reduction in HR
• preferred treatment in hypertensive patients with bradycardia and reduced cardia reserve
• low membrane-stabilizing effect
• moderate lipid solubility

• 2nd generation
• Cardioselective (B1 > B2)
• t1/2 - 6-9 hrs
• very hydrophilic, little CNS
• No local anesthetic & no sympmimic effects
• Uses: hypertension (conjuction with a diuretic); angina; arrhythmias
• B1 selective caution with asthma

• 2nd gen. B1 > B2
• t1/2 - 3-4 hrs
• moderate lipid sol
• first pass effect, varible plasma [ ]
• no sympath activity
• local anesthetic at high doses
• Uses: hypertension, mild heart failure
• arrythmias
• use caution in asthma

• 2nd gen B-blocker
• B1 > B2
• t1/2 - 10 min degraded by esterases in RBC
• low lipid sol
• no local anesth
• Use: emerency treatment of supraventricular tachycardia, arrhytmias associated thyrotoxicosis, and perioperactive hypertension

• 3rd gen - nonselective also comp blocker at a1
• symimic act. partial B2 agonist effects
• inhibits neuronal uptake of NE
• t1/2 4-5 hrs
• extensive first pass = low bioavail
• VD (a1-block, B2 agonist) & loss of reflex tachycardia
• Use: hypertension

• 3rd gen nonselective a1 antagonist as well
• t1/2 7-10 hrs
• moderate lipid sol
• no sympath
• VD
• an antioxidant - antihypertensive unit
• Uses: hypertension, mild to severe congestive heart failure, myocardia Ischemia

• Bradycardia (all of them)
• bronchospasm (esmolol, metoprolol, atenolol)
• dyspnea, wheezing
• sudden withdrawal = angina, tachycardia, cardia arrhymias
• Dec myocardial contraction and excitibility
• Heptotoxicity- labet.
• alteration of plasma lipids

all beta antagonist

propanolol, timolol, pindolol, atenolol, metoprolol, esmolol, labetalol, carvedilol,

Basically all of them

all except labetalol, carvedilol, and pidolol

propranolol and timolol

1st generation - Nonspecific - blocks both B1 & B2

2nd generation - more selective for B1 > B2

3rd generation - nonspecific so block both B1 & B2 but also a1 receptors

consider use of one with sympathomimetic activity

epi alone increases contractile force due to activation of b1 rec. inc in BP due a1 and inc in HR due to B1

propranolol blocks b1 and b2 receptors. Epi can only bind to a1 so BP response is greater now. no epi reversal.