Role of oxidative stress in angiotensin-induced hypertension

被引:165
作者
Reckelhoff, JF
Romer, JC
机构
[1] Mayo Clin, Dept Physiol & Biophys, Rochester, MN 55905 USA
[2] Univ Mississippi, Med Ctr, Dept Physiol & Biophys, Jackson, MS 39216 USA
关键词
isoprostanes; endothelin; spontaneous hypertension; renovascular hypertension; sodium balance;
D O I
10.1152/ajpregu.00491.2002
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Infusion of ANG II at a rate not sufficient to evoke an immediate vasoconstrictor response, produces a slow increase in blood pressure. Circulating levels of ANG II may be within ranges found in normotensive individuals, although inappropriately high with respect to sodium intake. When ANG II levels are dissociated from sodium levels, oxidative stress (OXST) occurs, which can increase blood pressure by several mechanisms. These include inadequate production or reduction of bioavailability of nitric oxide, alterations in metabolism of arachidonic acid, resulting in an increase in vasoconstrictors and decrease in vasodilators, and upregulation of endothelin. This cascade of events appears to be linked, because ANG II hypertension can be blocked by inhibition of any factor located distally, blockade of ANG II, OXST, or endothelin. Such characteristics are shared by other models of hypertension, such as essential hypertension, hypertension induced by reduction in renal mass, and renovascular hypertension. Thus these findings are clinically important because they reveal 1) uncoupling between ANG II and sodium, which can trigger pathological conditions; 2) the various OXST mechanisms that may be involved in hypertension; and 3) therapeutic interventions for hypertension developed with the knowledge of the cascade involving OXST.
引用
收藏
页码:R893 / R912
页数:20
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