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. 2013 Apr 10;304(12):R1096–R1106. doi: 10.1152/ajpregu.00367.2012

Fig. 5.

Fig. 5.

ANG II infusion attenuates baseline nitric oxide (NO) and NMDA-induced NO production in dissociated PVN cells. A: representative images of 4-amino-5-methylamino-2′,7′-difluorofluorescein diacetate (DAF-FM) fluorescence in PVN neurons of saline-recipient mouse are shown. NMDA increased NO-dependent fluorescence. Scale bar in A and B = 20 μm. B: representative images of DAF-FM fluorescence in PVN neurons from an ANG II-recipient mouse are shown. NMDA reduced NO-dependent fluorescence in PVN cells of ANG II-recipient mice. C: PVN cells from ANG II-infused mice have reduced NO production compared with PVN cells of mice receiving saline; *P < 0.05, using unpaired t-test. D: effect of NMDA on the time course of NO-dependent fluorescence in isolated PVN cells from saline and ANG II-treated mice; **P < 0.01 using an unpaired t-test. E: NMDA increases NO-dependent fluorescence in PVN cells of saline-infused mice, an effect prevented by the nitric oxide synthase inhibitor LNNA (100 μmol/l). **P < 0.01, using ANOVA and Tukey's test. F: NMDA reduces NO-dependent fluorescence in PVN cells of ANG II-treated mice. The suppression of NO formation is reversed by coapplied NOX2 peptide inhibitor gp-91ds-tat (1 μmol/l). **P < 0.01, using ANOVA and Tukey's test.