β receptors are classified into three subclasses: β₁, β₂, and β₃. β₁ receptors are primarily located in the heart and kidneys. When they get activated, they increase heart rate, contractility, and renin release. This process enhances blood pressure and aids in stress management. In contrast, β₂ receptors are situated mainly in the lungs, blood vessels, and skeletal muscles. Upon activation, they trigger smooth muscle relaxation, causing bronchodilation and vasodilation. This widens airways and blood vessels, improving oxygen delivery to tissues, reducing airway resistance, and aiding respiration. Beta antagonists, or beta-blockers, block beta-receptor sites by competing with norepinephrine and epinephrine. They are categorized as nonselective and selective. Nonselective beta-blockers target both β₁ and β₂ receptors, while selective ones focus solely on β₁ receptors. Nonselective beta-blockers like propranolol inhibit β₁ receptor activity in hypertensive patients, reducing heart rate, contraction force, and renin release. As a result, peripheral resistance, blood volume, and blood pressure decrease. However, due to its nonselective nature, propranolol inhibits the β₂-mediated bronchodilation, which can lead to increased airway resistance. This exacerbates respiratory conditions in asthma or chronic obstructive pulmonary disease (COPD). Selective beta-blockers such as metoprolol and atenolol decrease the risk of unwanted bronchoconstriction. Their specificity for β₁ receptors makes them cardioselective. Unlike nonselective blockers, which can cross the blood-brain barrier and cause CNS-related side effects due to their high lipophilicity, selective beta-blockers have low lipophilicity. They are less likely to impact the central nervous system.