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. 2002 Sep 6;544(Pt 3):883–896. doi: 10.1113/jphysiol.2002.021972

Figure 5. Effect of ACh on subcellular endothelial NOS (eNOS) distribution.

Figure 5

Hamster cheek pouches were superfused with buffer (control) or with 10 μm or 100 μm ACh for 3 min, homogenised and submitted to subcellular fractionation. Western blots were revealed by chemiluminescence to detect eNOS, Na+,K+-ATPase, or anti-coat protein beta (β-COP) content in the microsomal fraction (M), cytosolic fraction (C), heavy membrane/Golgi-enriched fraction (G) and total homogenate (T). A, distribution of eNOS in a representative series of blots obtained from one out of four similarly treated groups. Protein load per lane: M, 30 μg; C, 140 μg; G, 30 μg; T, 80 μg. ACh-treated tissues showed a marked decrease in microsomal eNOS content and an equivalent increase in the Golgi-enriched fraction. B, distribution of Na+,K+-ATPase and β-COP in one out of three similarly treated hamster cheek pouches. Protein load per lane: M, 40 μg; G, 40 μg. Application of ACh failed to affect the distribution of these proteins, which are markers for plasma (Na+,K+-ATPase) and Golgi (β-COP) membranes.