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.