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Am J Physiol Heart Circ Physiol 279: H1220-H1227, 2000;
0363-6135/00 $5.00
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Vol. 279, Issue 3, H1220-H1227, September 2000

Amlodipine inhibits thapsigargin-sensitive CA2+ stores in thrombin-stimulated vascular smooth muscle cells

Olivier Stepien and Pierre Marche

Département de Pharmacologie, Université René Descartes and Centre National de la Recherche Scientifique, Unité Mixte de Recherche 8604, Faculté de Médecine, 75015 Paris, France

Ca2+ channel blockers, such as amlodipine, inhibit vascular smooth muscle cell (VSMC) growth through interactions with targets other than L-type Ca2+ channels. The effects of amlodipine on Ca2+ movements in thrombin- and thapsigargin-stimulated VSMCs were therefore investigated by determining the variations of intracellular free Ca2+ concentration in fura 2-loaded cultured VSMCs. Results indicated that 10-1,000 nM amlodipine inhibited 1) thrombin-induced Ca2+ mobilization from a thapsigargin-sensitive pool and 2) thapsigargin-induced Ca2+ responses, including Ca2+ mobilization from internal stores and store-operated Ca2+ entry. These effects of amlodipine do not involve L-type Ca2+ channels and could not be reproduced with 100 nM isradipine, diltiazem, or verapamil. The inhibition by amlodipine of Ca2+ mobilization appears therefore to be a specific property of the drug, in addition to its Ca2+ channel-blocking property. It is suggested that amlodipine acts in this capacity by interacting with Ca2+-ATPases of the sarcoplasmic reticulum, thus modulating the enzyme activity. This mechanism might participate in the inhibitory effect of amlodipine on VSMC growth.

calcium channel blockers; calcium mobilization; vascular smooth muscle cell growth


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