The document discusses the pharmacology and uses of beta blockers, which are drugs that competitively block beta adrenergic receptors to manage cardiovascular conditions. It details their effects on the heart, blood vessels, and respiratory system, highlighting potential adverse effects and drug interactions. Key uses include treating hypertension, angina, myocardial infarction, and other conditions, while cautioning against their use in asthma and respiratory issues.

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

5. pharmacological actions
CARDIOVASCULAR SYSTEM:
a. Heart:
b-Blockers depress all the cardiac properties
i. Decrease heart rate (negative chronotropic effect).
ii. Decrease the force of myocardial contractility (negative inotropic
effect).
iii. 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

6. 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.

7. 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

8. 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

9. 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.

10. 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

11. 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.

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