Abstract

Introduction

Materials & Methods

Results

Discussion & Conclusion

References

Discussion
Board

An important unresolved issue in hypertension research is the mechanism for organ damage during the development of the syndrome. Reactive oxygen species, such as superoxide anion radicals (O2-), hydrogen peroxide (H2O2), hydroxyl radicals (•OH) and others, may play a critical role in the pathogenesis of hypertension, as well as conditions such as atherosclerosis, stroke and myocardial infarction for which hypertension is a significant risk factor. Oxygen free radicals may affect both vascular resistance, by inactivating nitric oxide (NO) and causing arteriolar vasoconstriction and elevation of peripheral resistance, and may serve as trigger mechanisms for lesion formation.

We will discuss here some recent evidence which suggests that an overproduction of oxygen free radicals may be involved in the development of human hypertension as well as hypertension in animal models such as the spontaneously hypertensive rat (SHR) and the Dahl hypertensive rat. Although the cellular source of excess oxygen free radical production remains largely speculative, intravital animal studies have suggested the endothelial cell as a potential source. Within the endothelial cell, xanthine oxidase, NAPDH and the mitochondria are all capable of producing oxygen free radicals.

We will discuss specifically the involvement of xanthine oxidase derived oxygen radicals in the SHR and Dahl model of hypertension. Xanthine oxidase can be chronically inhibited using a tungsten (sodium tungstate, Na2WO4), enriched diet and we examine its influence on free radical production in microvascular endothelium and blood pressure.

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