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(Hypertension. 2005;46:259.)
© 2005 American Heart Association, Inc.

Editorial Commentaries

Growing Old, Angiotensin II, Cardiac Hypertrophy, and Death

Making the Connection With p66^Shc

From the Departments of Medicine and Medical Physiology, Cardiovascular Research Institute, The Texas A&M University System Health Science Center, College of Medicine; Scott & White; Central Texas Veterans Health Care System, Temple, Tex.

Correspondence to George W. Booz, PhD, FAHA, The Cardiovascular Research Institute, The Texas A&M University System Health Science Center, College of Medicine, 1901 South 1st St, Building 205, Temple, TX 76504. E-mail gbooz@medicine.tamhsc.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Hypertension and aging have similar effects on the structure and function of blood vessels and the heart. Both commonly result in decreased vascular compliance, endothelial dysfunction, and left ventricular (LV) hypertrophy and stiffness. Moreover, the risk of cardiovascular disease, including hypertension, increases exponentially with age in those >40 years of age. Therefore, one might surmise that hypertension and aging have some cause in common. The idea that angiotensin II (Ang II) might be the "missing link" was suggested by reports that renin-angiotensin system (RAS) inhibitors, in addition to being effective in treating cardiovascular and renal diseases, protect the cardiovascular system, kidney, and brain against the harmful effect of aging.¹ Although findings based on angiotensin-converting enzyme inhibitors and the Ang II type 1 receptor blocker losartan should be interpreted with caution because of extra-RAS actions, evidence linking Ang II to increased collagen content and fibrosis of the aged heart is persuasive.² Intriguingly, in light of the article by Graiani et al in this issue,³ the mitochondria from hearts of rats chronically treated with losartan were found to have increased NO synthase (NOS) activity and decreased hydrogen peroxide formation compared with controls, suggesting that blocking the action of Ang II could offset the deleterious effect of aging on cardiac mitochondrial function and integrity.⁴

But Ang II has never been a major interest of aging research, which has focused recently on the oxidative stress experienced by aging cells because of increased reactive oxygen species (ROS) formation.⁵ Mitochondria represent a major source for this . . . [Full Text of this Article]