Figure 2.

Quantification of hypervascularization of CRFR2-mutant tissues. (a and b) Microfil casts after tissue digestion of CRFR2 control and mutant tissues. (a) Kidney, control is on left, CRFR2 mutant is on right (arrows indicate renal artery). (b) Intestine, control is on top, CRFR2 mutant is on bottom (arrows indicate mesenteric artery). (Scale bars represent 0.5 mm.) (c and d) Quantification of Microfil casts for comparison of weight of tissues (c) from CRFR2 control (white bars) or mutant (black bars) mice after proteinase K digestion, and cross-sectional diameter (d) of large conductance vessels showing fold increase in size of CRFR2-mutant vessels compared with control vessels. For the kidney, the renal artery was measured; for the gastrointestinal (GI) tract, the mesenteric artery was measured; and for the brain, the cerebral surface vessels were measured. Stom, stomach. Data are mean ± SEM; n = 3; ∗, P < 0.05; ∗∗, P < 0.01. (e–j) Sectioned tissues of Microfil casts for testicular artery (e and f), spleen (g and h), and cerebral cortex (i and j), showing increased vascular density in the CRFR2-mutant mice (f, h, and j) compared with control (e, g, and i). Arrows indicate cerebral vessels in CRFR2 control (i) and mutant (j) mouse brains, demonstrating increased size in CRFR2 mutant mice. (Scale bars represent 0.2 mm.) (k) Quantification of vessel counts in cerebral cortex. Wt, wild type; Mut, CRFR2 mutant. Data are mean ± SEM; n = 3; ∗, P < 0.05.