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Eur J Pharmacol. 1999 Jan 29;366(1):61-71.

Ca2+ buffering action of sarcoplasmic reticulum on Bay k 8644-induced Ca2+ influx in rat femoral arterial smooth muscle.

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  • 1Department of Pharmacology, Nagoya City University Medical School, Japan.


We examined the Ca2+ buffering action of sarcoplasmic reticulum during the stimulation of arterial smooth muscle with Bay k 8644 [methyl-1,4-dihydro-2,6-dimethyl-3-nitro-4-(2-trifluoromethylphenyl)-pyr idine-5-carboxylate]. The effects of Bay k 8644 on tension and cellular Ca2+ level were first determined in endothelium-denuded strips of rat femoral artery. The Ca2+ buffering action was examined by using cyclopiazonic acid and thapsigargin to inhibit Ca2+-ATPase of sarcoplasmic reticulum and ryanodine to deplete Ca2+ stored in sarcoplasmic reticulum. The addition of Bay k 8644 (0.3-300 nM) to the resting strips almost failed to cause a contraction. When the strips were preincubated with 10 microM cyclopiazonic acid, Bay k 8644 induced a concentration-dependent contraction that is antagonized by nifedipine. The maximum contraction induced by Bay k 8644 in the presence of cyclopiazonic acid was comparable to the maximum contraction induced by 65.9 mM K+-depolarization and the ED50 value for Bay k 8644 was around 5 nM. Similar results were obtained when the strips were preincubated with 30 nM thapsigargin or 10 microM ryanodine. Bay k 8644 also induced a strong contraction when the extracellular K+ concentration was elevated. During the stimulation with 100 nM Bay k 8644, the Ca2+ influx was increased. We conclude that in rat femoral arterial smooth muscle, (1) the Ca2+ influx induced by Bay k 8644 is completely buffered by Ca2+ uptake into the sarcoplasmic reticulum, and (2) this sarcoplasmic reticulum can buffer a large amount of Ca2+ that induces a maximum contraction.

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