title: Blocking effect of salvianolic acid A on calcium channels in isolated rat ventricular myocytes.
abstract: OBJECTIVE
  To study the effect of salvianolic acid A (SAA) on L-type calcium current (I-CaL) in isolated ventricular myocytes of Sprague-Dawley rats.
  
  
  METHODS
  SAA powder was dissolved in normal Tyrode's solution to reach the concentrations of 1, 10, 100, and 1000 μmol/L. The traditional whole-cell patch-clamp recording technique was employed to evaluate the effects of SAA on I-CaL in single ventricular myocytes which were prepared by Langendorff perfusion apparatus from Sprague-Dawley rats.
  
  
  RESULTS
  SAA (1, 10, 100, and 1000 μmol/L) inhibited I-CaL peak value by 16.23%±1.3% (n=6, P<0.05), 22.9%±3.6% (n=6, P<0.05), 53.4%±3.0% (n=8, P<0.01), and 62.26%±2.9% (n=6, P<0.01), respectively. SAA reversibly inhibited I-CaL in a dose-dependent manner and with a half-blocking concentration (IC(50)) of 38.3 μmol/L. SAA at 100 μmol/L elevated the I-V curve obviously, and shifted the half-active voltage (V(0.5)) from (-15.78±0.86) mV to (-11.24 ±0.77) mV (n=6, P<0.05) and the slope (K) from 5.33±0.74 to 4.35±0.74 (n=6, P>0.05). However, it did not alter the shapes of I-V curve, steady-state inactivation curve, or recovery from inactivation curve.
  
  
  CONCLUSIONS
  SAA inhibited I-CaL in a dose-dependent manner. It shifted the steady-state activation curve to a more positive voltage, which indicated that the drug affected the activated state of calcium channels, and suggested that the Ca(2+) antagonistic effect of SAA be beneficial in the treatment of myocardial ischemia reperfusion injury.
authors.affiliation: The Laboratory Research Center, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
authors.forename: Bao
authors.initials: B
authors.lastname: Wang
authors.forename: Jian-xun
authors.initials: JX
authors.lastname: Liu
authors.forename: Hong-xu
authors.initials: HX
authors.lastname: Meng
authors.forename: Cheng-ren
authors.initials: CR
authors.lastname: Lin
mesh_terms: D000818:Animals; D002109:Caffeic Acids / Q000737:chemistry / Q000494:pharmacology*; D002121:Calcium Channel Blockers / Q000737:chemistry / Q000494:pharmacology*; D020746:Calcium Channels, L-Type / Q000502:physiology*; D004305:Dose-Response Relationship, Drug; D004365:Drugs, Chinese Herbal / Q000737:chemistry / Q000494:pharmacology*; D007773:Lactates / Q000737:chemistry / Q000494:pharmacology*; D017202:Myocardial Ischemia / Q000188:drug therapy / Q000503:physiopathology; D032383:Myocytes, Cardiac / Q000187:drug effects* / Q000502:physiology; D018408:Patch-Clamp Techniques; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000188:drug therapy / Q000503:physiopathology
chemical_list: D002109:Caffeic Acids; D002121:Calcium Channel Blockers; D020746:Calcium Channels, L-Type; D004365:Drugs, Chinese Herbal; D007773:Lactates; C066201:salvianolic acid A