β1 receptors in the heart and kidneys regulate cardiac output and renin release. Under stress conditions, the activation of these receptors by catecholamines increases blood pressure and promotes optimal organ function. β2 receptors in lungs and blood vessels induce smooth muscle relaxation, promoting bronchodilation and vasodilation, enhancing oxygen delivery and easing respiration. β-blockers competitively block these receptors; nonselective ones target both β1 and β2-receptors, while selective ones bind to β1 receptors. In hypertensive patients, nonselective β-blockers, like propranolol, inhibit β1 receptor activity, reducing cardiac output and renin release, lowering blood volume and pressure. Propranolol's nonselective nature also blocks β2 receptors, worsening bronchoconstriction in hypertensive patients with respiratory disorders. In such cases, cardioselective β-blockers, such as metoprolol and atenolol, are preferred. They specifically target β1 receptors of the heart, effectively reducing blood pressure without inducing airway constriction. Atenolol's limited blood-brain barrier entry minimizes CNS side effects, contrasting propranolol's active penetration, leading to potential CNS-related side effects.