In your discussion of the mechanism by which ACE-inhibitors, AT1-antagonists and calcium antagonists cause normalization of small artery structure, you suggest that this is being mediated through calcium, as a final common pathway. Another possibility is that these drugs have a similar effect because they are all vasodilators. This contrasts to beta-blockers without intrinsic activity, where peripheral resistance remains high for a considerable time, the bp reduction being due to reduction of cardiac output. Thus the drug treatment causes the vessels to dilate, and the vessels the adapt structurally to the new diameter. The pathways involved may be calcium-dependent or -independent. Could you comment on this please?