Fig. 4.

Genetic deletion of the endothelial GC-A receptor in mice causes pulmonary vascular remodelling together with mild perivascular inflammation under normoxic conditions and, more, after chronic hypoxia. Lung sections were immunostained for SMC α-actin or for lymphocyte common antigen (CD45). a Quantification of the relative numbers of fully (F), partially (P) and non (N) muscularized arterioles and b of perivascular CD45-positive cells per field demonstrated enhanced pulmonary vascular remodelling and perivascular inflammatory infiltration in EC GC-A KO mice under normoxia and after hypoxia (n = 8 mice per group). *P < 0.01 vs. controls; ^† P < 0.01 vs. normoxia