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The Influence of β1‐Adrenergic Receptor Genotype of Renal Sodium Handling and Blood Pressure Response to Angiotensin Receptor Blockers in Hypertension Patients

The β1‐adrenergic receptors (ADRB1) are found primarily in the heart and the juxtaglomerular cells of the kidneys. Within the kidneys, ADRB1 promote the release of renin and the activation of the renin‐angiotensin‐aldosterone system (RAAS). The RAAS plays a primary role in the regulation of renal Na+ handling and blood pressure (BP). Specifically, within the RAAS, aldosterone preferentially increases renal tubular luminal Na+ transport via increasing apical Na+ permeability. As a result, systolic and diastolic blood pressures are impacted by RAAS activity. Additionally, baseline renin levels predict Na+ sensitivity. Multiple polymorphisms of the ADRB1 have been identified as including a glycine (Gly) for arginine (Arg) substitution at amino acid 389. The Gly389 polymorphism is associated with a lower risk of hypertension and increased plasma renin levels compared to the Arg389 polymorphism. The influence of ADRB1 genotype on renin release and blood pressure suggests the functional role it may play in renal Na+ handling.