Drugs online research references
Br J Pharmacol. 1995 Mar;114(6):1165-70.
Ca2+ entry activated by emptying of intracellular Ca2+ stores in ileal smooth muscle of the rat.
Ohta T, Kawai K, Ito S, Nakazato Y.
Department of Pharmacology, Faculty of Veterinary Medicine, Hokkaido University, Sapporo, Japan.
1. The effects of depletion of intracellular Ca2+ stores on muscle tension and the intracellular Ca2+ concentration ([Ca2+])i were studied in fura-2 loaded longitudinal smooth muscle cells of the rat ileum. 2. After exposure to a Ca(2+)-free solution, application of Ca2+ caused a small contraction and a rise in [Ca2+]i, both of which were potentiated when the muscle was challenged with carbachol or caffeine before the addition of Ca2+. 3. Cyclopiazonic acid (CPA), a specific inhibitor of sarcoplasmic reticulum Ca(2+)-ATPase, dose-dependently decreased tension development and the rises in [Ca2+]i induced by carbachol and caffeine in the Ca(2+)-free solution, but conversely increased the Ca(2+)-induced responses even in the presence of the voltage-dependent Ca2+ channel blockers, methoxyverapamil and nifedipine. 4. The contraction and rise in [Ca2+]i evoked by Ca2+ gradually declined with time after removal of CPA, while the reverse was the case for the responses to carbachol and caffeine. 5. The Ca(2+)-induced contraction and rise in [Ca2+]i in the presence of CPA were inhibited by the replacement of Na+ with K+ or Cs+, and by the addition of Cd2+, Ba2+, Ni2+ or La3+. 6. The influx of Mn2+ was much greater in extent in the presence of CPA than in its absence. 7. These results suggest that the emptying of intracellular Ca2+ stores may activate Ca2+ influx not associated with voltage-dependent Ca2+ channels in the rat ileal smooth muscle.
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J Cell Biochem. 2000 Mar;77(2):200-12.
Role of protein kinase C in 1,25(OH)(2)-vitamin D(3) modulation of intracellular calcium during development of skeletal muscle cells in culture.
Capiati DA, Vazquez G, Tellez Inon MT, Boland RL.
Departamento de Biologia, Bioquimica y Farmacia, Universidad Nacional del Sur, 8000 Bahia Blanca, Argentina.
Regulation of muscle cell Ca(2+) metabolism by 1, 25-dihydroxy-vitamin D(3) [1,25(OH)(2)D(3)] is mediated by the classic nuclear mechanism and a fast, nongenomic mode of action that activates signal transduction pathways. The role of individual protein kinase C (PKC) isoforms in the regulation of intracellular Ca(2+) levels ([Ca(2+)](i)) by the hormone was investigated in cultured proliferating (myoblasts) and differentiated (myotubes) chick skeletal muscle cells. 1,25(OH)(2)D(3) (10(-9) M) induced a rapid (30- to 60-s) and sustained (>5-min) increase in [Ca(2+)](i) which was markedly higher in myotubes than in myoblasts. The effect was suppressed by the PKC inhibitor calphostin C. In differentiated cells, PKC activity increased in the particulate fraction and decreased in cytosol to a greater extent than in proliferating cells after 5-min treatment with 1,25(OH)(2)D(3). By Western blot analysis, these changes were correlated to translocation of the PKC alpha isoform from cytosol to the particulate fraction, which was more pronounced in myotubes than in myoblasts. Specific inhibition of PKC alpha activity using antibodies against this isoform decreased the 1, 25(OH)(2)D(3)-induced [Ca(2+)](i) sustained response associated with Ca(2+) influx through voltage-dependent calcium channels. Neomycin, a phospholipase C (PLC) inhibitor, blocked its effects on [Ca(2+)](i), PKC activity, and translocation of PKC alpha. Exposure of myotubes to 1,2-dioleyl-rac-glycerol (1,2-diolein), also increased [Ca(2+)](i), PKC activity, and the amount of PKC alpha associated with the particulate fraction. Changes in [Ca(2+)](i) induced by diolein were inhibited by calphostin C and nifedipine. The results indicate that PKC alpha activation via PLC-catalyzed phosphoinositide hydrolysis is part of the mechanism by which 1, 25(OH)(2)D(3) regulates muscle intracellular Ca(2+) through modulation of the Ca(2+) influx pathway of the Ca(2+) response to the sterol. Copyright 2000 Wiley-Liss, Inc.
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J Cardiovasc Pharmacol. 1992;19 Suppl 2:S60-2.
Action of metoprolol, enalapril, diltiazem, verapamil, and nifedipine on cell growth of vascular smooth muscle cells.
Sachinidis A, Ko Y, Graack GK, Wieczorek AJ, Vetter H.
Medizinische Universitats-Poliklinik Bonn, Germany.
The influence of nifedipine, verapamil, diltiazem, metoprolol, and enalapril on the basal and angiotensin II (Ang II)-induced elevation of [3H]thymidine incorporation into vascular smooth muscle cell (VSMC) DNA was examined. Our results from four independent experiments, each performed in triplicate, are summarized by calculating the half-maximal inhibitory concentration (IC50) of the drugs. Nifedipine, verapamil, and diltiazem had IC50 values of 2.3 +/- 0.7 x 10(-6), 3.5 +/- 0.3 x 10(-6), and 6.6 +/- 2.8 x 10(-6) M, respectively. Metoprolol had an IC50 value of 49 +/- 16 x 10(-6) M, whereas enalapril was completely ineffective. All drugs used had no influence on the basal cell [3H]thymidine incorporation. This in vitro study allows one to conclude that the calcium-entry blockers can inhibit the Ang II-induced cell growth and thus may have beneficial effects on the development and regression of vascular growth, which is associated with the pathogenesis of cardiovascular diseases.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1377309&dopt=Abstract
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