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Diabetes is strongly associated with an accelerated rate of development of atherosclerosis1. Evidence suggests that elevated serum glucose levels may contribute to atherogenesis in diabetic patients by promoting oxidation of lipoproteins, propagation of free radicals, and production of advanced glycation end-products (AGE)2 3 4. However, the exact mechanisms of how hyperglycemia accelerates atherogenesis are not understood.

Hypertension may predispose to the development of thrombotic vascular disease by promoting interactions between circulating blood monocytes (mo) and vascular endothelial cells (EC). The adherence of mo from spontaneously hypertensive (SHR), normotensive Wistar-Kyoto (WKY) and Sprague-Dawley (SD) rats to cultures of activated and untreated homologous cerebral microvascular EC was examined. There were no significant differences in the percent of monocytes from all three strains adhering to untreated EC. Mo binding was inhibited (approx. 50%) by antibodies against (β2-integrin molecules (CD 11 a, CD 11 b, CD l 8) and intercellular adhesion molecule-1 (ICAM-l). Treatment of EC with LPS, IL–1β, TNFα or IFNγ dose-dependently upregulated mo adhesion. The level of syngeneic and allogeneic mo adhesion to stimulated SHR EC was significantly more upregulated than was observed with identically treated WKY or SD EC (p

The pathogenesis of arteriosclerosis appears to involve a sequence of critical events that are based on the interaction of cellular (platelets, monocyte-macrophages) and noncellular (lipoproteins) blood elements with the arterial wall.