What is the primary mechanism of action of β blockers in the treatment of hypertension and angina?

The primary mechanism of action of β blockers in the treatment of hypertension and angina involves the decrease of heart rate, contractility, and cardiac output. β blockers work by blocking the β-adrenergic receptors in the heart and other tissues. This blockage leads to a reduction in the effects of catecholamines, such as adrenaline, which typically increase heart rate and force of myocardial contraction.

By decreasing heart rate and contractility, β blockers effectively lower cardiac output, which diminishes the workload on the heart and is particularly beneficial in managing conditions like hypertension and angina. This results in a reduction of myocardial oxygen demand, improving clinical symptoms in patients with angina and helping to lower blood pressure in hypertensive patients.

In relation to the other options, increasing heart rate and contractility would contradict the primary therapeutic goals of using β blockers. Additionally, while β blockers can indeed influence the renin-angiotensin system, they primarily reduce renin secretion rather than increase it, and they do not play a role in enhancing aqueous humor secretion, which is more related to other classes of medications like carbonic anhydrase inhibitors. The focus of β blockers is specifically on reducing the heart's workload and managing blood pressure through their depressant effects on the