β1-receptors are primarily located in the heart and kidneys. In cardiac myocytes, these receptors interact with neurotransmitters released by the sympathetic nervous system during heightened activity or danger. As a result, β1-receptors get activated, initiating a series of biochemical processes. Excessive activation of beta receptors due to chronic stress can abnormally increase heart rate and contractility, resulting in high blood pressure or hypertension. To counteract this, β1-blockers competitively inhibit catecholamines from binding to β1-receptors. This inhibition reduces the effect of β1-receptor activation on the heart, leading to a decrease in heart rate and force of contraction.
Eventually, the heart's workload is reduced, and blood pressure decreases. In the kidneys, overactivation of β1-receptors enhances renin production from the juxtaglomerular cells of the afferent arteriole. This increase in renin enzyme concentration leads to more angiotensinogen being converted to angiotensin I, which results in higher angiotensin II production – a potent vasoconstrictor. Angiotensin II narrows blood vessels and elevates blood pressure. Increased angiotensin II levels trigger the adrenal gland to produce more aldosterone hormone. This hormone causes the kidneys to retain sodium and water, increasing blood volume and pressure. By blocking β1-receptors, renin production decreases, subsequently reducing angiotensin II production. This reduction allows blood vessels to relax and widen, lowering blood flow resistance and decreasing blood pressure.
