title: [The effect of angiotensin-converting enzyme inhibitors and aldosterone receptor blockers on cardiac function in calcium-overload rats].
abstract: OBJECTIVE
  To observe the effect of angiotensin-converting enzyme inhibitors (ACEI) and aldosterone receptor blockers on cardiac function to explore the mechanism of cardiac function descending and myocardial injury in calcium-overload rats.
  
  
  METHODS
  Calcium-overload in rat was induced by administration of Vitamin D3 plus nicotine. To Estimate the extent of calcium-overload by calcium content. Angiotension II and aldosterone levels in the myocardia were measured by radioimmunoassay. Cardiac function (+/- LVdp/dt, LVESP and LVEDP) were measured by Powerlab. The malondialdehyde (MDA) content, activities of lactate dehydrogenase (LDH) and creatine kinase (CPK) were measured by biochemistry.
  
  
  RESULTS
  Calcium content increased by 3.2-, 5.8 -fold in myocardial and artery, compared with controls. VDN-treated survivors showed lower + LVdp/dt(max) and -LVdp/dt(max) values, by 27% and 34%, respectively (both P < 0.01). Higher LVESP, and LVEDP by 42 % and 32% (P < 0.01); heart rate and mean arterial pressure were not significantly altered (P > 0.05). The lipid peroxidation products MDA and conjugated diene in myocardia were increased 22% (P < 0.01), 68% (P < 0.05) (P < 0.05), respectively. The plasma activity of CPK and LDH was greatly increased by 4.5-and 3.1-fold (P < 0.01), respectively. ACEI and spironolactone obviously relieved degree of calcium-overload and improved cardiac function and myocardial injury(P < 0.01). Calcium content in myocardia and artery was lower 44%, 39% and 57%, 34%. Lower MDA by 20%, 30%, lower conjugated diene by 44%, 35% than calcium-overload group. The plasma activity of CPK and LDH were obviously decreased 28%, 34% and 20%, 27%, compared with calcium-overload group.
  
  
  CONCLUSIONS
  Calcium-overload could lead to cardiac function descending and myocardial injury in calcium-overload rats by VDN. ACEI and spironolactone could reduce calcium-overload in myocardial and ameliorate cardiac function and decrease myocardial injury.
authors.affiliation: Department of Pathophysiology, Yunyang Medical College, Shiyan 442000, China. shengyingwu@163.com
authors.forename: Sheng-Ying
authors.initials: SY
authors.lastname: Wu
authors.forename: Xiong
authors.initials: X
authors.lastname: Wang
authors.forename: Yan
authors.initials: Y
authors.lastname: Chen
authors.forename: Ji-Xia
authors.initials: JX
authors.lastname: Pen
authors.forename: Li
authors.initials: L
authors.lastname: Li
authors.forename: Yong-Fen
authors.initials: YF
authors.lastname: Qi
authors.forename: Chao-Shu
authors.initials: CS
authors.lastname: Tang
mesh_terms: D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology*; D000818:Animals; D002118:Calcium / Q000009:adverse effects*; D003402:Creatine Kinase / Q000378:metabolism; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D015227:Lipid Peroxidation; D008297:Male; D008315:Malondialdehyde / Q000032:analysis; D000451:Mineralocorticoid Receptor Antagonists; D009206:Myocardium / Q000378:metabolism*; D009538:Nicotine / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013148:Spironolactone / Q000494:pharmacology*; D014807:Vitamin D / Q000494:pharmacology
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D000451:Mineralocorticoid Receptor Antagonists; D014807:Vitamin D; D013148:Spironolactone; D008315:Malondialdehyde; D009538:Nicotine; D007770:L-Lactate Dehydrogenase; D003402:Creatine Kinase; D002118:Calcium