title: Blood Pressure and the Renal Actions of AT2Receptors.
abstract: Angiotensin type-2 receptors (AT2Rs) in the renal proximal tubule inhibit sodium (Na+) reabsorption by inducing renal cyclic GMP formation and internalizing and inhibiting major Na+ transporters Na+-H+ exchanger-3 (NHE-3) and Na+/K+ATPase (NKA). Instead of angiotensin II (Ang II), angiotensin III (Ang III) is the predominant endogenous agonist for this response. Exogenous non-peptide AT2R agonist Compound-21 induces natriuresis and lowers blood pressure (BP) in normal and Ang II-infused hypertensive rodents. Spontaneously hypertensive rats (SHR; both pre-hypertensive and hypertensive) have defective natriuretic responses to Ang III, suggesting a defect in AT2R-mediated natriuresis in SHR that leads to hypertension. The mechanisms of deficient AT2R-mediated natriuresis in SHR are unknown but could involve either pre-receptor or receptor/post-receptor defects.
authors.affiliation: Division of Endocrinology and Metabolism, Department of Medicine, University of Virginia Health System, Charlottesville, VA, 22908, USA. rmc4c@virginia.edu.
authors.forename: Robert M
authors.initials: RM
authors.lastname: Carey
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects*; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000503:physiopathology*; D007687:Kidney Tubules, Proximal / Q000187:drug effects / Q000503:physiopathology*; D009318:Natriuresis / Q000187:drug effects; D011918:Rats, Inbred SHR; D044139:Receptor, Angiotensin, Type 2 / Q000819:agonists*; D012964:Sodium / Q000378:metabolism
chemical_list: D044139:Receptor, Angiotensin, Type 2; D012964:Sodium
keywords: AT2 receptor; Angiotensin receptor; Blood pressure; Hypertension; Natriuresis; Sodium excretion