title: [Effect of pinacidil on rat myocardial calcium regulation].
abstract: To understand the effect of pinacidil on rat myocardial Ca(2+)regulation.
  
  
  
  After baseline measurement and a period of equilibrium, myocytes were randomly allocated to one of 4 treatment groups: Control group (8 myocytes): incubation in Lactate Ringer's solution at 24 degrees C for 2 hours; K group (8 myocytes): incubation in Lactate Ringer's solution containing 16 mmol/L potassium at 24 degrees C for 2 hours; K+P group (8 myocytes): incubation in Lactate Ringer's solution containing potassium 16 mmol/L and pinacidil 50 micromol/L at 24 degrees C for 2 hours; K+P+G group (8 myocytes): incubation in Lactate Ringer's solution containing potassium 16 mmol/L, pinacidil 50 micromol/L and glibenclamide 10 micromol/L at 24 degrees C for 2 hours. After each incubation, myocytes were resuspended in cell culture media at the same temperature and intracellular [Ca(2+)](i) and SR Ca(2+) release were measured.
  
  
  
  The amplitude percent of [Ca(2+)](i) transient evoked by electrical stimulation in the K group was significantly decreased to 67.05% - 80.11% compared to 90.27% - 95.57% in the K+P group during reperfusion after ischemia (P<0.01). The percent amplitude of the [Ca(2+)](i) transient evoked by the rapid application of 10 mmol caffeine in the K group myocyte was approximately 112.00%+/-16.93% compared with that of the [Ca(2+)](i) transient evoked by electrical stimulation. However, in the K+P group myocyte the peak amplitude of the caffeine induced Ca(2+) release was 173.15%+/-26.01% compared with electrical stimulation (P<0.01). The duration of transient evoked by caffeine in K+P group (3.20+/-0.71 ms was significantly shorter than that in K group (3.93+/-0.46) ms (P<0.05).
  
  
  
  Cardioplegic arrest with simultaneous activation of KATP channels preserves rat myocardial Ca2+ by inducing sarcoplasmic reticulum Ca(2+) release and by alteration of Na(+)-Ca(2+) exchanger to better maintain [Ca(2+)](i) homeostasis.
authors.affiliation: Department of Thoracic and Cardiolvasular Surgery, The Affiliated Children' s Hospital, College of Medical Sciences, Zhejiang University, Hangzhou 310003, China.
authors.forename: Ru
authors.initials: R
authors.lastname: Lin
authors.forename: Man-li
authors.initials: ML
authors.lastname: Kang
authors.forename: Chun-mei
authors.initials: CM
authors.lastname: Cao
authors.forename: Qiang
authors.initials: Q
authors.lastname: Xia
authors.forename: Qiang
authors.initials: Q
authors.lastname: Shu
authors.forename: Ze-wei
authors.initials: ZW
authors.lastname: Zhang
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism*; D005260:Female; D006321:Heart / Q000187:drug effects*; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D020110:Pinacidil / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012964:Sodium / Q000378:metabolism
chemical_list: D020110:Pinacidil; D012964:Sodium; D002118:Calcium