Blood pressure responses following challenge with angiotensin II or AT1 receptor blockade in wild-type and RGS2-deficient mice. (a) Time courses of blood pressure increase (change in MAP ± SEM, mmHg) following intraarterial administration of pressor doses of angiotensin II to RGS2-deficient mice (n = 6; filled squares) and wild-type mice (n = 6; open squares). (b) Time courses of blood pressure decrease (change in MAP ± SEM, mmHg) following AT1 receptor blockade with candesartan in wild-type (n = 6; open squares) and rgs2^–/– mice (n = 6; filled squares). (c) Time course of blood pressure decrease [(MAP – MAP_final)/(MAP_initial – MAP_final)] ± SEM following AT1 receptor blockade in wild-type (n = 7; open squares) and rgs2^–/– mice (n = 7; filled squares) that were pretreated with a pressor dose of angiotensin II to elevate blood pressures to similarly high starting values (systolic blood pressure = 160–170 mmHg). The results shown in each panel are representative of more than ten experiments performed with each genotype. The changes in blood pressure for wild-type and rgs2^–/– mice were compared at each time point. Statistically significant differences are indicated (*P < 0.01, **P < 0.002). (d) Western blot analysis of AT1 receptors in aortic extracts. AT1 receptor expression in aortae from wild-type rats and rgs2^+/+ (WT), rgs2^+/–, and rgs2^–/– mice is indicated (upper panel). Antibody specificity was verified by probing of an identical blot with primary antibody that first had been incubated with blocking peptide (lower panel).