American Society of Anesthesiologists

Fig. 6. The dose-dependent effects of sevoflurane (SEV) on angiotensin (Ang) II–stimulated phosphorylation of Ca2+-dependent protein kinase C α (cPKC-α) in rat aortic smooth muscle. The rat endothelium-denuded aortas were incubated to 0, 1.7, 3.4, or 5.1% sevoflurane for 15 min and were frozen 4 min after application of angiotensin II (10−7m). Phosphorylated cPKC-α band was detected using a specific antibody with Western blotting. The levels of phosphorylated cPKC-α were expressed as a percentage of cPKC-α band density. *P < 0.05, **P < 0.01 versus the value in the presence of angiotensin II and 0% sevoflurane (n = 4). p-cPKC-α= phosphorylated cPKC-α.

Fig. 6. The dose-dependent effects of sevoflurane (SEV) on angiotensin (Ang) II–stimulated phosphorylation of Ca²⁺-dependent protein kinase C α (cPKC-α) in rat aortic smooth muscle. The rat endothelium-denuded aortas were incubated to 0, 1.7, 3.4, or 5.1% sevoflurane for 15 min and were frozen 4 min after application of angiotensin II (10⁻⁷m). Phosphorylated cPKC-α band was detected using a specific antibody with Western blotting. The levels of phosphorylated cPKC-α were expressed as a percentage of cPKC-α band density. *P < 0.05, **P < 0.01 versus the value in the presence of angiotensin II and 0% sevoflurane (n = 4). p-cPKC-α= phosphorylated cPKC-α.

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