Regulation of L-type inward calcium channel activity by captopril and angiotensin II via the phosphatidyl inositol 3-kinase pathway in cardiomyocytes from volume-overload hypertrophied rat hearts.

@article{Alvin2011RegulationOL,
  title={Regulation of L-type inward calcium channel activity by captopril and angiotensin II via the phosphatidyl inositol 3-kinase pathway in cardiomyocytes from volume-overload hypertrophied rat hearts.},
  author={Zikiar V. Alvin and Graham G. Laurence and Bernell R. Coleman and Aiqiu Zhao and Majd Hajj-Moussa and Georges E Haddad},
  journal={Canadian journal of physiology and pharmacology},
  year={2011},
  volume={89 3},
  pages={206-15}
}
Heart failure can be caused by pro-hypertrophic humoral factors such as angiotensin II (Ang II), which regulates protein kinase activities. The intermingled responses of these kinases lead to the early compensated cardiac hypertrophy, but later to the uncompensated phase of heart failure. We have shown that although beneficial, cardiac hypertrophy is associated with modifications in ion channels that are mainly mediated through mitogen-activated protein (MAP) kinase and phosphatidylinositol 3… CONTINUE READING

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