title: Effect of tetrandrine on free intracellular calcium in cultured calf basilar artery smooth muscle cells.
abstract: OBJECTIVE
  To study the effects of tetrandrine (Tet) on extracellular Ca2+ influx and intracellular Ca2+ release in cultured calf basilar artery smooth muscle cells.
  
  
  METHODS
  Free intracellular calcium was examined by a system of measurement of AR-CM-MIC, using Fura 2-AM as a fluorescent indicator.
  
  
  RESULTS
  In the presence of extracellular Ca2+ 1.3 mmol/L, no significant effect of Tet on resting [Ca2+]i was found. KCl 20, 40, and 60 mmol/L triggered a sustained rise in [Ca2+]i, pretreatment with Tet inhibited the elevation of [Ca2+]i induced by KCl in concentration-dependent manner, Tet at high concentration (100 micromol/L) almost abolished the rise of [Ca2+]i evoked by KCl. Caffeine 10 mmol/L only produced a transient increase of [Ca2+]i, which spontaneously declined back to resting levels. Tet 10-30 micromol/L had no effect on caffeine-induced [Ca2+]i transient peak. Tet at high concentration (100 micromol/L), however, reduced the [Ca2+]i transient peak induced by caffeine. Phenylephrine (PE) 10 mmol/L produced a rapid transient peak and a distinct sustained elevation in [Ca2+]i in the presence of extracellular Ca2+. In the absence of extracellular Ca2+ containing egtazic acid (EGTA), PE only produced a rapid transient peak in [Ca2+]i. Pretreatment of Tet (10-100 micromol/L) inhibited the sustained elevation in [Ca2+]i induced by PE in a concentration-dependent manner. However, only 100 micromol/L of Tet inhibited the transient peak in [Ca2+]i induced by PE both in the presence of extracellular Ca2+ 1.3 mmol/L and in the absence of extracellular Ca2+ containing EGTA.
  
  
  CONCLUSIONS
  Tet inhibited the Ca2+ influx from the extracellular site via voltage-activated Ca2+ channel and PE-receptor-operated Ca2+ channel. At a high concentration, Tet may inhibit the Ca2+ release from sarcoplasmic reticulum (SR) or refilling of intracellular calcium store in cerebral artery smooth muscle cells.
authors.affiliation: Department of Pharmacology, Nanjing Medical University, Nanjing 210029, China. Binwang@njmu.edu.cn.
authors.forename: Bin
authors.initials: B
authors.lastname: Wang
authors.forename: Ji-Gao
authors.initials: JG
authors.lastname: Xiao
mesh_terms: D000470:Alkaloids / Q000494:pharmacology*; D000818:Animals; D001488:Basilar Artery / Q000166:cytology*; D044182:Benzylisoquinolines / Q000494:pharmacology*; D002110:Caffeine / Q000037:antagonists & inhibitors; D002118:Calcium / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D015220:Calcium Channels / Q000187:drug effects*; D002417:Cattle; D002478:Cells, Cultured; D009131:Muscle, Smooth, Vascular / Q000187:drug effects* / Q000378:metabolism; D032389:Myocytes, Smooth Muscle / Q000166:cytology / Q000378:metabolism; D010656:Phenylephrine / Q000037:antagonists & inhibitors; D011189:Potassium Chloride / Q000037:antagonists & inhibitors
chemical_list: D000470:Alkaloids; D044182:Benzylisoquinolines; D002121:Calcium Channel Blockers; D015220:Calcium Channels; D010656:Phenylephrine; C009438:tetrandrine; D002110:Caffeine; D011189:Potassium Chloride; D002118:Calcium