Leptin Inhibits the Proliferation of Vascular Smooth Muscle Cells Induced by Angiotensin II through Nitric Oxide-Dependent Mechanisms
Figure 5
Impaired NO production and NOS activity and increased NADPH oxidase expression in aortic VSMCs from hypertensive rats. Bar graphs show (a) the accumulation of NOx in the culture media and (b) the NOS activity of aortic VSMCs from control Wistar rats and spontaneously hypertensive rats (SHR) stimulated with leptin (10 nmol/l) for 30 minutes. (c) Basal expression of Nox2, a subunit of the NADPH oxidase, in VSMCs from control Wistar rats and SHR. Data are expressed as mean SEM ( = 10). Differences between groups were analysed by two-way ANOVA (a, b) or Student’s t test (c). In case of interaction between factors (strain and leptin treatment), differences between groups were analysed by one-way ANOVA followed by Dunnet’s test *.05, ** .01 versus control response in unstimulated cells (a, b) or VSMCs from control rats (c).
