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fact, we found that the reduction in BP of obese hypertensives treated with ACE inhibition correlated with the improvement of insulin’s ability to suppress fatty acids (N 511, r5 -0.73, p,0.01). These data raised the possibility that tissue (adipocyte) ACE contributes to obesity hypertension in part through adverse effects on lipid (fatty acid) metabolism. It is tempting to speculate that improvement of insulin’s fatty acid lowering action contributed to the reduction in new onset diabetes in HOPE. Angiotensin synergistically enhances the production of reactive oxygen species in vascular smooth muscle cells (VSMCs) stimulated with oleic acid, an effect no antagonized by Vitamin E. The reactive oxygen species are critical signaling molecules in the migration and proliferation of VSMCs stimulated with oleic acid and angiotensin. The expression of ACE and AT1 receptors is increased in atherosclerotic plaque, especially the shoulder regions, which are vulnerable to rupture and incite thrombosis. Proteinases, which destabilize the plaque, are present in the shoulder areas and activated by oxidative stress. The local amplification of angiotensin production (ACE) and action (AT 1 receptors) in concert with the lipid abnormalities of the cluster would serve to accelerate vascular remodeling and the associated vascular catastrophes by augmenting oxidative stress, which is probably not attenuated by Vitamin E. The highly beneficial outcomes with drugs that interrupt the RAS in high risk subjects are consistent with the basic science data. Paradoxically, the benefits of ACE inhibition in HOPE may have been mediated by antioxidant actions, whereas Vitamin E was ineffective. Utilization of agents which inhibit the RAS among high risk, insulin-resistant subjects prior to the development of diabetes mellitus and hypertension may prevent these manifestations of the cluster and the vascular complications that ensue.

An analysis of recent clinical trials and their impact on JNC VI guidelines