iNOS- or IFNγ-deficient mice are resistant to the hypotensive effects of neutropenia. (A) iNOS knockout mice are resistant to the hypotensive effects of neutrophil depletion. Blood pressure measurements were carried out in iNOS−/− C57BL/6 mice with/without administration of RB6-8C5 (n ≥ 3, mean ± SEM). Controls are age- and sex-matched wild-type C57Bl/6. (B) Induction of iNOS during neutropenia in wild-type mice. Thoracic aortic sections from control and neutropenic wild-type mice (day 3) were sectioned and stained for iNOS. Representative sections are shown for each condition. (C) Pixel intensity was determined after fluorescence staining of aortic sections (n = 3 separate aortae, with 25 determinations per aorta). (D) IFNγ knockout mice are resistant to the hypotensive effects of neutrophil depletion. Blood pressure measurements in IFNγ−/− Balb/C mice with/without administration of RB6-8C5 (n ≥ 6, mean ± SEM). (E) IFNγ−/− mice do not show decreased PE constriction following RB6-8C5 administration. PE-induced constriction responses in thoracic aortae from control IFNγ−/− mice and IFNγ−/− mice depleted of neutrophils for 3 days (n ≥ 6, mean ± SEM). Aortic ring functional responses were determined.