INTERPLAY OF REACTIVE OXYGEN SPECIES AND NITRIC OXIDE IN THE PATHOGENESIS OF EXPERIMENTAL LEAD-INDUCED HYPERTENSION

• Published in: Clinical and experimental pharmacology & physiology Vol. 34; no. 9; pp. 920 - 925
• Main Authors: Vaziri, ND, Khan, M
• Format: Journal Article
• Language: English
• Published: Melbourne, Australia Blackwell Publishing Asia 01.09.2007
• Subjects: Animals; atherosclerosis; Blood Pressure; cardiovascular disease; Cyclic GMP - metabolism; Disease Models, Animal; endothelial dysfunction; Guanylate Cyclase - metabolism; Hypertension - chemically induced; Hypertension - metabolism; Hypertension - physiopathology; Lead; NADPH Oxidases - metabolism; Nephritis, Interstitial - chemically induced; Nephritis, Interstitial - metabolism; Nephritis, Interstitial - physiopathology; nitric oxide; Nitric Oxide - metabolism; Nitric Oxide Synthase - metabolism; Oxidative Stress; Reactive Oxygen Species - metabolism; Receptors, Cytoplasmic and Nuclear - metabolism; Soluble Guanylyl Cyclase; toxic exposure
• ISSN: 0305-1870; 1440-1681
• DOI: 10.1111/j.1440-1681.2007.04644.x

SUMMARY 1 Lead is a common environmental and industrial toxin that can cause a variety of acute and chronic illnesses. For example, chronic exposure to low levels of lead has been shown to raise arterial pressure and promote renal and cardiovascular complications. 2 Several mechanisms have been identified by which chronic lead exposure can cause hypertension and cardiovascular disease. In recent years, increasing evidence has emerged pointing to the role of oxidative stress as a major mediator of lead‐induced hypertension. 3 The present article provides an overview of the published studies on this subject.