β₁ receptors are primarily found in the heart and kidneys.

In cardiac myocytes, these receptors respond to stress-induced neurotransmitters, such as catecholamines.

Chronic stress can overstimulate these receptors, elevating the heart rate and blood pressure.

β₁-blockers can inhibit the binding of catecholamines to β₁ receptors, reducing their effects on the heart and decreasing the heart rate and, eventually, the blood pressure.

In the kidneys, overactivation of β₁ receptors increases renin production from the juxtaglomerular cells of the afferent arteriole.

Increased renin converts angiotensinogen to angiotensin I, subsequently raising angiotensin II levels. This vasoconstrictor narrows blood vessels and increases blood pressure.

Angiotensin II also promotes aldosterone production, leading to sodium and water reabsorption and increasing blood volume and blood pressure.

Blocking β₁ receptors reduces renin and aldosterone production, decreasing sodium and water reabsorption and lowering blood volume and pressure.