ß-receptor blocking agents make the postsynaptic target cells of the sympathetic nervous system less sensitive to stimulation. β1-receptors are mainly present on the excitable cells in the myocardium. β2-receptors can be found in the walls of the respiratory tract and certain blood vessels. Stimulation of the β-receptors results in tachycardia, increased cardiac output, increased velocity of conduction, and a shorter refractory period. β2-receptor stimulation evokes dilation of bronchioles, vasodilation, and tachycardia, as well as increased glycogenolysis and lipolysis. Conversely, blocking these receptors results in decreased blood pressure, decreased cardiac contractile activity, decreased cardiac output and heart rate, decreased peripheral circulation, and constriction of bronchioles. All these effects reduce the oxygen demand of myocytes. Blockade of only β1-receptors results in primarily cardiovascular effects with little change in bronchial status. Non-selective β-blockers (e.g. propranolol and sotalol) block both β-receptors and thus also affect the respiratory system and glucose levels. Selective β1-blockers (e.g. metoprolol

and atenolol) are more or less specific for the β1-receptors. Most β-blockers have a good oral absorption, are metabolised in the liver, and are excreted via the kidneys. The plasma half-lives vary between 15 minutes and 22 hours. The therapeutic window is generally very wide. At high doses, the selectivity of β1-blockers is lost. Indications for the use of β-blockers are angina pectoris, acute coronary syndromes, heart failure, hypertension, and certain arrhythmias. Certain β-blockers are also used for the treatment of other cardiovascular disorders. Selective β-blockers lead to fewer adverse effects than non-selective β-blockers. Both groups of drugs can cause dyspnoea and asthma attacks. More general side effects include fatigue, insomnia, and dizziness. Lipophilic β-blockers such as metoprolol can easily cross the blood-brain barrier and evoke depression, fear, and nightmares. They are preferred to prevent adrenergically-induced arrhythmias. Atenolol and sotalol are hydrophilic ß-blockers.


Mr B is under treatment with low-dose atenolol for his hypertension. His BP was about 145/95 mm Hg at his last three visits. In addition, Mr B complains of fatigue. How will you manage Mr B's hypertension?


β-blockers are used for the treatment of angina for all the following reasons EXCEPT:


What is true about propranolol?