First, it is true that in cell culture experiments, 20% FCS will result in changes in cell phenotype (contractile to synthetic) and cell hyperplasia. Nevertheless, in our organ culture system, FCS alone does not induce any obvious phenotypic changes and certainly does not promote DNA synthesis; we found that changes in phenotype (in the form of loss of smooth muscle cell marker proteins) could be attributed to loss of stretch stimuli (ie in vessels maintained without pressure, compared to vessels maintained at 80 mmHg) rather to the presence of serum. These discrepancies between cell and organ culture systems may reflect on the importance of the environment (3-D structure, complex extracellular matrix) in determining the phenotypic or synthetic outcome of specific treatments used in culture.
Second, I'm afraid that 10 mmHg should rather be labeled as 50 mmHg. Nonetheless, there are no observed differences in MAP kinase activity between vessels maintained at 10, 50 or 80 mmHg in our organ culture system. 150 mmHg is used as an in vitro model of vessel stretch which may be encountered during hypertension.
Third, there does not appear to be a significant role for endothelial cells in conveying mechanical stress, at least not in the case of pulsatile stretch. Indeed, in vessels where the endothelium was stripped (using a Fogarty catheter) without overstretching, the MAP kinase activation in response to pulsatility was identical to that seen in non-denuded vessels. The equivalent experiment was not done for steady stretch, however, and it will be interesting to investigate a potential role for endothelial cells in that situation. Nevertheless, one must keep in mind the possibility that endothelial cells may contribute to MAP kinase activation, but that this response be masked by that of the more abundant vascular smooth muscle cells.