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The Roles of cAMP and G Protein Signaling in Oxidative Stress-Induced Cardiovascular Dysfunction

  • Soumya Saha
  • Zhenquan Jia
  • Dongmin Liu
  • Hara P. MisraEmail author
Chapter
Part of the Oxidative Stress in Applied Basic Research and Clinical Practice book series (OXISTRESS)

Abstract

Cyclic adenosine monophosphate (cAMP) is a second messenger that plays a vital role in numerous biological processes. It serves as an intracellular signal transducer in many different organisms, exerting its effect through gene expression. In addition to its effects on intermediary metabolism, it has profound effects on cellular events, including growth stimulation, cell differentiation, and development. It mediates the action of many hormones acting through the cAMP response element (CRE) at gene levels. The levels of intracellular cAMP are regulated by Adenylyl cyclase (AC) and phosphodiesterase that catalyze the formation and breakdown of cAMP, respectively. Abnormalities in cAMP levels have been implicated in the pathogenesis of vascular diseases including hypertension. Increased levels of cAMP have been shown to have anti-inflammatory and tissue-protective effects. Reactive oxygen species (ROS) that cause oxidative stress have been shown to play a major role in the initial stage of cardiovascular diseases, including hypertension, where the role of cAMP has been implicated. Although the role of cAMP-signaling during hypertension is well known, its effects on oxidative stress protection are not fully understood. Two different signaling pathways have been suggested where cAMP could play a major role in causing hypertension: (1) lowering the cAMP levels, by angiotensin II, induces ROS production that leads to over expression of Giα protein, which consequently exerts hypertensive effects, and (2) increased levels of cAMP is known to attenuate the NADPH oxidase activity in cells, resulting in decreased oxidative stress, which, in turn, would decrease hypertension. However, in hyperglycemic state, it was proposed that an altered Gi protein expression causes accumulation of cAMP that leads to oxidative stress, thus resulting in hypertension. Regardless of the actual mechanism of action, it is apparent that cAMP and G protein signaling are associated with oxidative stress and play an important role in the pathogenesis of hypertension and hyperglycemia.

Keywords

cAMP CVD G protein Oxidative stress 

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Copyright information

© Springer Science+Business Media, LLC 2011

Authors and Affiliations

  • Soumya Saha
  • Zhenquan Jia
  • Dongmin Liu
  • Hara P. Misra
    • 1
    Email author
  1. 1.Edward Via Virginia College of Osteopathic MedicineBlacksburgUSA

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