Trends in Cardiovascular Medicine
Volume 16, Issue 4 , Pages 109-114 , May 2006

Nitric-Oxide-Induced Vasodilatation: Regulation by Physiologic S-Glutathiolation and Pathologic Oxidation of the Sarcoplasmic Endoplasmic Reticulum Calcium ATPase

  • Richard A. Cohen

      Affiliations

    • Corresponding Author InformationAddress correspondence to: Richard A. Cohen, MD, Director, Vascular Biology Unit, Boston University Medical Center, 650 Albany Street X708, Boston, MA 02118. Tel.: (+1) 617-638-7115/7113; fax: (+1) 617-638-7115/7113.
    • ,
  • Takeshi Adachi

References 

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  3. Adachi T, Matsui R, Xu S, et al. Antioxidant improves smooth muscle sarco/endoplasmic reticulum Ca(2+)-ATPase function and lowers tyrosine nitration in hypercholesterolemia and improves nitric oxide-induced relaxation. Circ Res. 2002;90:1114–1121
  4. Adachi T, Pimentel DR, Heibeck T, et al. S-glutathiolation of Ras mediates redox-sensitive signaling by angiotensin II in vascular smooth muscle cells. J Biol Chem. 2004;279:29857–29862
  5. Adachi T, Weisbrod RM, Pimentel D, et al. S-glutathiolation by peroxynitrite activates SERCA during arterial relaxation by nitric oxide. A mechanism targeted by oxidants in vascular disease. Nat Med. 2004;10:1200–1207
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  15. Cohen RA. The potential clinical impact of 20 years of nitric oxide research. Am J Physiol. 1999;276:H1404–H1407
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PII: S1050-1738(06)00020-X

doi: 10.1016/j.tcm.2006.02.001

Trends in Cardiovascular Medicine
Volume 16, Issue 4 , Pages 109-114 , May 2006

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