Genetic inactivation of the B2 receptor in mice worsens two-kidney, one-clip hypertension: role of NO and the AT2 receptor.

Abstract

These results indicate that B2R inactivation selectively worsens the maintenance phase of 2K1C Goldblatt hypertension and support the notion that B2R-deficient mice exhibit an impaired ability to release NO in response to elevations of ANG II levels. Chronic administration of an AT2 receptor blocker did not modify the course of 2K1C Goldblatt hypertension in either B2R-/- or B2R+/+ mice. Therefore, the role of AT2 receptors in B2R-mediated protection against ANG II-dependent hypertension remains uncertain.