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Title: Pathogenesis of lead-induced hypertension: role of oxidative stress. Author: Vaziri ND. Journal: J Hypertens Suppl; 2002 Jun; 20(3):S15-20. PubMed ID: 12184052. Abstract: Chronic exposure to low levels of lead causes hypertension in humans and experimental animals. Several mechanisms have been shown to contribute to the pathogenesis of lead-induced hypertension: (1) avid oxidation and inactivation of endogenous nitric oxide (NO) by reactive oxygen species leading to functional NO deficiency; (2) increased sympathetic activity and circulating noradrenaline coupled with decreased vascular and elevated renal beta-adrenergic receptor density; (3) increased angiotensin-converting enzyme (ACE) activity and elevated plasma renin, angiotensin II and aldosterone levels; (4) heightened kininase I and kininase II activities; (5) possible increase in endothelin and thromboxane production; and (6) lead-mediated inhibition of vascular smooth muscle Na(+)-K+ ATPase leading to a rise in cellular Na+ and hence Ca2+ stores. This paper provides an overview of the epidemiology of lead-induced hypertension followed by a review of the available data on the above-mentioned topics.[Abstract] [Full Text] [Related] [New Search]