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 2Structures of aorta and renal vasculature in wild-type and RGS2-deficient mice. Histological analysis (hematoxylin-and-eosin or Verhoeff–Van Gieson elastin staining) of wild-type (
a,
c, and
e) and
rgs2–/– (
b,
d, and
f) mice. Aorta (
a and
b), renal interlobular arteries (
c and
d), and nonelastic arterioles of the renal cortex (
e and
f) are shown. (
g) Morphometric analysis of relative medial thickness (medial area/total area) of renal resistance vessels with diameters of 50–100 μm from wild-type,
rgs2+/–, and
rgs2–/– mice. Relative medial thickness of
rgs2 mutants differed significantly (*
P < 0.0001) from that of wild-type mice.
