Effect of SR 33805 on arterial smooth muscle cell proliferation and neointima formation following vascular injury.

@article{Dol1995EffectOS,
  title={Effect of SR 33805 on arterial smooth muscle cell proliferation and neointima formation following vascular injury.},
  author={Fred́eŕique Dol and Paul Schaeffer and Isabelle Lamarche and A M Mar{\'e}s and Pierre Chatelain and Jean-M. Herbert},
  journal={European journal of pharmacology},
  year={1995},
  volume={280 2},
  pages={
          135-42
        }
}
Effect of Azelnidipine on Angiotensin II-Mediated Growth-Promoting Signaling in Vascular Smooth Muscle Cells
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Interestingly, azelnidipine increased rather than decreased the later ERK peaks in cells treated with small interfering RNA against mitogen-activated protein kinase phosphatase-1, which provides new insight into the manner in which calcium channels exert an essential action in the AT1 receptor-mediated growth-promoting actions in VSMCs.
Calcium Channel Blocker Azelnidipine Enhances Vascular Protective Effects of AT1 Receptor Blocker Olmesartan
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It is suggested that azelnidipine could inhibit vascular injury at least partly independent of the inhibition of AT1 receptor activation and that azennidIPine could exaggerate the vascular protective effects of olmesartan, suggesting clinical possibility that the combination of CCB and ARB could be more effective in the treatment of vascular diseases.
Alteration of the [Ca2+]i‐force relationship during the vasorelaxation induced by a Ca2+ channel blocker SR33805 in the porcine coronary artery
TLDR
SR33805 caused an apparent leftward shift of the [Ca2+]i‐force relationship of the contraction induced by cumulative application of extracellular Ca2+ during 118 mM K+‐depolarization.
Calcium channel blockers, apoptosis and cancer: is there a biologic relationship?
  • R. Mason
  • Biology, Medicine
    Journal of the American College of Cardiology
  • 1999
Alteration of the [Ca(2+)](i)-force relationship during the vasorelaxation induced by a Ca(2+) channel blocker SR33805 in the porcine coronary artery.
TLDR
SR33805 caused an apparent leftward shift of the [Ca(2+)](i)-force relationship of the contraction induced by cumulative application of extracellular Ca(2+) during 118 mM K(+)-depolarization.
Proteomic analysis and comparison of intra- and extracranial cerebral atherosclerosis responses to hyperlipidemia in rabbits
TLDR
Differential protein expression levels (TPM1, HSP70 and α-smooth muscle actin) between intra- and extracranial cerebral arteries may facilitate the identification of novel biological markers for the diagnosis and treatment of cerebral arteriosclerosis.
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