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Propranolol is a medication of the beta blocker type. It is used to treat high blood pressure. It is used to prevent migraine headaches and to prevent further heart problems in those with angina or previous heart attacks. It is administered by oral route. Propranolol enters in the systemic circulation after 30 minutes and has a maximum effect between 60 and 90 minutes when adminietred by oral route. It is a non-selective beta blocker which works by blocking β-adrenergic receptors.
Propranolol should not be used in those with an already slow heart rate and most of those with heart failure. Quickly stopping the medication in those with coronary artery disease may worsen symptoms. It may worsen the symptoms of asthma. Greater care is recommended in those with liver or kidney problems. Propranolol has harmful effects on the foetus if taken during pregnancy. Its use during breastfeeding is probably safe but the baby should be monitored for side effects.
Propranolol was discovered in 1964. It is on the World Health Organization’s List of Essential Medicines. Propranolol is available as a generic medicine. The wholesale cost in the developing countries is between US$0.24 and US$2.16 per month.
Propranolol may be contraindicated in people with:
Reversible airways diseases, particularly asthma or chronic obstructive pulmonary disease (COPD)
Bradycardia (<60 beats/minute)
Sick sinus syndrome
Atrioventricular block (second- or third-degree)
Adverse drug reactions of beta blockers are
Mixed α1/β-antagonist therapy is also commonly associated with orthostatic hypotension. Carvedilol
therapy is commonly associated with edema. Due to the high penetration across the blood–brain barrier, lipophilic beta blockers such as propranolol and metoprolol are more likely than other less lipophilic beta blockers to cause sleep disturbances such as insomnia, vivid dreams and nightmares.
Adverse effects associated with β2-adrenergic receptor antagonist activity (bronchospasm, peripheral vasoconstriction, alteration of glucose and lipid metabolism) are less common with β1-selective (often termed “cardioselective”) agents but receptor selectivity diminishes at higher doses. Beta blockade is especially of the beta-1 receptor at the macula densa, inhibits renin release. Thus decreasing the release of aldosterone.
This causes hyponatremia and hyperkalemia.
Hypoglycemia can occur with beta blockade because β2-adrenoceptors normally stimulate glycogen breakdown (glycogenolysis) in the liver and pancreatic release of the hormone glucagon, which work together to increase plasma glucose. Therefore, blocking β2-adrenoceptors lowers plasma glucose. β1-blockers have fewer metabolic side effects in diabetic patients.
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