| 规格: | 98% |
| 分子量: | 220.25 |
| 包装 | 价格(元) |
| 10mg | 电议 |
| 25mg | 电议 |
| 50mg | 电议 |
| 100mg | 电议 |
| 200mg | 电议 |
| 500mg | 电议 |
Background:
S-Nitroso-N-acetyl-DL-penicillamine (SNAP) is a nitric oxide donor and acts as a stable inhibitor of platelet aggregation[1][2][3][4].
S-Nitroso-N-acetyl-DL-penicillamine (10 mM; 8 hours) induces toxicity of about 80% after 6 hours under normoxic conditions by releasing nitric oxide (NO)[1].S-Nitroso-N-acetyl-DL-penicillamine has a half-time about 6 hours in in isolated rat ventricular myocytes[3]. S-Nitroso-N-acetyl-DL-penicillamine (100 µM; 30 minutes) causes sustained decrease in the basal pHi in isolated rat ventricular myocytes[3]. Cell Viability Assay[1] Cell Line: Rat liver sinusoidal endothelial cells
SNAP (100μM, 300μM) causes small but significant increases of the electrically evoked [3H]-acetylcholine release in guinea-pig tracheal[4].
[1]. E. Salas, et al. Comparative pharmacology of analogues of S-nitroso-N-acetyl-DL-penicillamine on human platelets. Br J Pharmacol. 1994 Aug;112(4):1071-6. [2]. Ioannidis I, et al. Enhanced release of nitric oxide causes increased cytotoxicity of S-nitroso-N-acetyl-DL-penicillamine and sodium nitroprusside under hypoxic conditions. Biochem J. 1996 Sep 15;318 ( Pt 3):789-95. [3]. Pravdic D, et al. Effect of nitric oxide donors S-nitroso-N-acetyl-DL-penicillamine, spermine NONOate and propylamine propylamine NONOate on intracellular pH in cardiomyocytes. Clin Exp Pharmacol Physiol. 2012 Sep;39(9):772-8. [4]. Mang CF, et al. Modulation of acetylcholine release in the guinea-pig trachea by the nitric oxide donor, S-nitroso-N-acetyl-DL-penicillamine (SNAP). Br J Pharmacol. 2000 Sep;131(1):94-8.
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