Current Hypertension Reports

, Volume 6, Issue 4, pp 314–320

Lead-induced hypertension: Role of oxidative stress

  • Nosratola D. Vaziri
  • Domenic A. Sica

DOI: 10.1007/s11906-004-0027-3

Cite this article as:
Vaziri, N.D. & Sica, D.A. Current Science Inc (2004) 6: 314. doi:10.1007/s11906-004-0027-3


Chronic, low-level lead exposure causes hypertension in both animals and humans. The pathogenesis of leadinduced hypertension is multifactorial, including such diverse mechanisms as: inactivation of endogenous nitric oxide and downregulation of soluble guanylate cyclase by reactive oxygen species (ROS), leading to a functional deficiency in nitric oxide; heightened sympathetic activity and plasma norepinephrine together with depressed vascular and elevated renal β-adrenergic receptor density; elevated plasma angiotensin-converting enzyme (ACE) activity, plasma renin activity (PRA), angiotensin II (Ang-II), and aldosterone levels; increased kininase I and kininase II activities; lead-induced inhibition of vascular smooth muscle Na+-K+ ATPase, leading to a rise in cellular Na+ and, hence, Ca2+; and a possible rise in endothelin and thromboxane generation. In this article, we present an overview of the epidemiology and proposed underlying mechanisms of lead-induced hypertension.

Copyright information

© Current Science Inc 2004

Authors and Affiliations

  • Nosratola D. Vaziri
    • 1
  • Domenic A. Sica
    • 1
  1. 1.Division of Nephrology and HypertensionUniversity of California, Irvine, UCI Medical CenterOrangeUSA

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