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- W2069796959 abstract "Rho kinase (ROCK) and nitric oxide (NO) are important targets in cardiovascular diseases. Therefore, we investigated the possible influence of NO on Rho kinase (ROCK-2 isoform) expressions in cultured rat coronary microvascular endothelial cells. The cells were isolated from Wistar rats on a Langendorff system, and were incubated overnight (~16 h) with an NO generator, A-23187 (10−7 to 10-6 M), NO donors, such as sodium nitroprusside (10−7 to 10−6 M), glyceryl trinitrate (10−7 to 10−6 M), 2,2′-(hydroxynitrosohydrazono)bis-ethanimine (10−7 to 10−6 M), and NaNO2 (10−4 to 10−3 M) or a nitric oxide synthase (NOS) inhibitor, NG-nitro-L-arginine methylester (2×10−4 M), or two ROCK inhibitors, (+)-(R)-trans-4-(1-aminoethyl)- N-(4-pyridyl) cyclohexanecarboxamide dihydrochloride monohydrate (Y-27632, 10-5 M) and fasudil (10-5 M) in the absence or presence of thrombin (4 U/mL). ROCK-2 and endothelial NOS (eNOS) expressions were detected by Western blotting. Moreover, nitrite/nitrate levels were detected by Griess method in the presence of the ROCK inhibitors. The NO donors and the NO generator had no significant effects on ROCK-2 expression. Y-27632 and fasudil did not alter eNOS expression and NO production. Nitrite/nitrate levels were 4.4 ± 0.32 μM in control and 4.0 ± 0.93 μM and in Y-27632 group. These results demonstrate that prolong NO donation could not suppress the expression of ROCK-2 protein, and the ROCK inhibitor did not change e-NOS expression and NO production in the cultured rat coronary microvascular endothelial cells." @default.
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- W2069796959 date "2008-02-01" @default.
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- W2069796959 title "Nitric Oxide Does Not Downregulate Rho-Kinase (ROCK-2) Expression in Rat Coronary Endothelial Cells" @default.
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- W2069796959 doi "https://doi.org/10.1097/fjc.0b013e31815e4089" @default.
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