Hypertension and prolonged vasoconstrictor signaling in RGS2-deficient mice
J. Clin. Invest. Scott P. Heximer, et al. 111:445 doi:10.1172/JCI15598 [
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Figure 3Blood 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).
