Skip to main content
. 2000 Jun 15;525(Pt 3):761–770. doi: 10.1111/j.1469-7793.2000.00761.x

Figure 7. The upregulation of ETB mRNA expression by arterial levels of shear stress is mediated by NO and PKC, but not by tyrosine kinases.

Figure 7

In HUVEC exposed to long-term (24 h) laminar shear stress, endothelin receptor type B (ETB) mRNA expression was determined by standard-calibrated, competitive RT-PCR. Application of shear stress increased ETB receptor mRNA expression in a dose-dependent manner (A). In further studies, HUVEC were exposed to arterial levels of shear stress (ss) for 24 h in the presence or absence of inhibitors of ecNOS (L-N: 100 μM L-NAME, similar results with up to 500 μM L-NAME, not shown), of protein kinase C (RO: 1 μM RO-31-8220), or of tyrosine kinase (HA: 1 μM herbimycin A) (B). Values are expressed as percentage of control without shear stress; n= 4; * P < 0.05 vs. control without shear stress (con) (static condition: open bar, shear stress: hatched bars). ETB mRNA expression was determined using standard-calibrated, competitive RT-PCR. Values are given as percentage of static control (for L-N, RO and HA: control with inhibitor and dextran, but without shear stress), as means ±s.e.m.; n= 3; * P < 0.05 vs. control without shear stress (con) (static condition: open bar, shear stress: hatched bars).