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
        }
}
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19 Citations
Background Citations
4
Methods Citations
1

19 Citations

The calcium inhibitor SR33805 reduces intimal formation following injury of the porcine carotid artery.
Effect of Azelnidipine on Angiotensin II-Mediated Growth-Promoting Signaling in Vascular Smooth Muscle Cells
TLDR
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 antagonist verapamil inhibits neointimal formation and enhances apoptosis in a vascular graft model.
Calcium Channel Blocker Azelnidipine Enhances Vascular Protective Effects of AT1 Receptor Blocker Olmesartan
TLDR
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.
Differential effects of Ca2+ channel blockers on Ca2+ transients and cell cycle progression in vascular smooth muscle cells.
Cholesterol, calcium and atherosclerosis: is there a role for calcium channel blockers in atheroprotection?
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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References

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In vitro characterization of a novel Ca2+ entry blocker: SR 33805.
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The calcium antagonist nifedipine inhibits arterial smooth muscle cell proliferation.
Antiatherogenic activity of FR34235 (Nilvadipine), a new potent calcium antagonist. Effect on cuff-induced intimal thickening of rabbit carotid artery.
Regulation of Ca2+ transport by platelet-derived growth factor-BB in rat vascular smooth muscle cells.
TLDR
During prolonged stimulation by PDGF-BB, both Ca2+ influx and efflux are stimulated, resulting in a new intracellular Ca2+.
Long‐Term Effects of Verapamil on Aortic Smooth Muscle Cells Cultured in the Presence of Hypercholesterolemic Serum
TLDR
The presently reported results support the possibility that verapamil may impede the develipment of atheroma formaiton by reduction of smooth muscle cell proliferation in cholesterol-fed rabbits.
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Role of platelets in smooth muscle cell proliferation and migration after vascular injury in rat carotid artery.
TLDR
It is concluded that platelets do not play a role in the initiation of smooth muscle cell proliferation after injury by balloon catheter but may regulate their movement into the intima.
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TLDR
It is concluded that VSMC FC content plays a role in regulating cellular calcium homeostasis, both under basal conditions and in response to selected agonists.
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