Fig. 4.

Partial thiol depletion prevents oral nitrite from attenuating the blood pressure responses to angiotensin II and blunts oral nitrite-induced increases in plasma concentrations of nitrosylated species, in total protein and PKC nitrosylation in the vessels. Panel A shows the increases in mean arterial blood pressure (MAP) after infusion of angiotensin II (0.03, 0.1, 0.3, 1.0 and 3.0 μg/kg, i.v.) in rats pretreated with the glutathione synthase inhibitor buthionine sulfoximine (BSO) 1.4 mmol/kg every 12 h, i.p., and with oral nitrite (15 mg/kg) or vehicle for five days. BSO pretreatment blunted the effects of oral nitrite, which were found in control animals treated with vehicle instead of BSO and are shown in Fig. 1A). Panels B and C show the concentrations of nitrite and nitrosylated species (RXNO), respectively, in plasma from rats pretreated with vehicle or nitrite, and with BSO or BSO and nitrite for five days. Panel D shows a representative SDS/PAGE gel stained with Coomassie Blue to quantify total protein nitrosylation in aortic samples from the four experimental groups using the SNO-RAC method (“I” corresponds to input: total protein; “o” corresponds to output: nitrosylated protein). The bar graphic shows the quantification of total nitrosylated proteins in the aortic samples. Panel E shows the quantification of PKC expression in the aortas from the four experimental groups using Western blotting analysis and show a representative marking to quantify PKC nitrosylation. Panel F show the quantification of PKC nitrosylation in aortic samples from the four experimental groups. Data are shown as mean ± S.E.M. (n = 5–10/group). *P < 0.05 versus Vehicle. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)