Beta blockers - pharmacology

beta-Blockers competitively block the beta-mediated actions of catecholamines and other adrenergic agonists.

1. BETA BLOCKERS - PHARMACOLOGY Dr. S P SRINIVAS NAYAK Assistant Professor, SUCP Dept. of Pharmacy Practice.

2. BETA RECEPTORS ACTIVATION OF BETA.1 RECEPTORS Heart : Cardiac stimulation. Kidney : Promote renin release . ACTIVATION OF BETA 2-RECEPTORS Liver : Stimulation of glycogenolysis . Skeletal muscle: Contraction. Lungs: Bronchodilation , uterine relaxation (pregnant), bladder smooth muscles relaxation Uptake of K+ into cells . ACTIVATION OF BETA 3-RECEPTORS causes lipolysis

3. Beta blockers beta-Blockers competitively block the beta-mediated actions of catecholamines and other adrenergic agonists . Also called Beta adrenergic antagonists Beta blockers Beta receptor blockers Sympatholytic agents

4. pharmacological actions CARDIOVASCULAR SYSTEM: Heart : b-Blockers depress all the cardiac properties Decrease heart rate (negative chronotropic effect). Decrease the force of myocardial contractility (negative inotropic effect ). Decrease cardiac output . B . Blood vessels: Blockade of beta 2-receptors of the blood vessels initially may cause rise in peripheral vascular resistance due to the unopposed alpha 1-action. But continued will reduce peripheral resistance, AND REDUCE BP C. Kidneys : blocks renin release and decreases HTN

5. Respiratory system: Blockade of B 2-receptors in bronchial smooth muscle can produce severe bronchospasm in patients with COPD and asthma. Therefore , B2-blockers should be avoided in patients with asthma and COPD.

6. SKELETAL MUSCLE: On chronic use, B-blockers may cause skeletal muscle weakness and tiredness due to blockade of B 2-receptors of the skeletal muscle and blood vessels supplying it. They also reduce stress-induced tremors. DOC in hyperthyroidism

7. Metabolic effects: b -Blockers inhibit glycogenolysis and delay recovery from hypoglycaemia . They also mask the warning signs and symptoms of hypoglycaemia . Therefore, b-blockers should be used cautiously in diabetics on hypoglycaemic agents. Chronic use of nonselective b-blockers decreases high-density lipoprotein (HDL) cholesterol and low-density lipoprotein (LDL) cholesterol ratio, which may increase the risk of coronary artery disease

8. Pharmacokinetics Propranolol(all other b-blockers) is highly lipid soluble and is well absorbed from GI tract. However, the bioavailability of propranolol is low because of its extensive first-pass metabolism . It is highly bound to plasma proteins; has large volume of distribution; freely crosses BBB, and metabolites are excreted in urine.

9. ADRs CVS: Bradycardia , heart block and may precipitate congestive heart failure in patients with low cardiac reserve. RESPIRATORY SYSTEM: Blockade of b2-receptors in the bronchial smooth muscle can cause severe bronchospasm in patients with asthma and COPD. CNS : Sleep disturbances, hallucinations, fatigue and mental depression Hypoglycaemia is common with non selective agents Withdrawal symptoms: Abrupt withdrawal of b-blockers after chronic use is dangerous because they can precipitate angina or frank myocardial infarction and even sudden death Muscle weakness tiredness

10. Drug interactions propranolol × verapamil : They produce additive cardiac depressant effects and may cause CCF, bradyarrhythmias , heart block or even cardiac arrest . Propranolol × lignocaine: Propranolol reduces the clearance of lignocaine by decreasing hepatic blood flow Insulin/sulfonylureas × b-blockers : Nonselective b-blockers inhibit glycogenolysis and delay recovery from hypoglycaemia propranolol × nonsteroidal antiinflammatory drugs (NSAIDs): NSAIDs by inhibiting prostaglandin synthesis, promote Na+ and water retention on chronic use. Thus, they decrease antihypertensive effect of b-blockers .

11. USES HTN ANGINA, MI CCF ARRHYTHMIA GLAUCOMA PHEOCROMOCYTOMA HYPERTHYROIDISM MIGRAINE ANXIETY