141887-34-5

To verify this hypothesis, B₂^-/- or wild-type mice (B₂^+/+) are administered a nonpeptide antagonist of Ang II type 1 (AT₁) receptors (A81988) from conception through 180 days of age. Untreated B₂^+/+ and B₂^-/- served as controls. Blood pressure (BP) and heart rate are monitored with the use of tail-cuff plethysmography at regular intervals. Ventricular weights, diameters, wall thickness, chamber volume, and myocardial fibrosis are measured at 40 and 180 days. No differences are observed in BP, heart rate, and cardiac weight and dimensions between treated and untreated B₂^+/+. The BP of AT₁ antagonist-treated B₂^-/- is reduced until 70 days; then, it increases to the levels found in untreated B₂^-/-. AT₁ receptor blockade results in a reduction in left ventricular mass, chamber volume, and wall thickness and abrogated myocardial fibrosis in B₂^-/-[2]. A81988 (A-81988) decreases the BP of Bk2r^-/- either in normosodic conditions or after sodium deprivation, whereas in Bk2r^+/+ it produces a modest decrease under hyposodic conditions only^[3].