title: Additional salutary effects of the combination of exercise  training and an angiotensin-converting enzyme inhibitor on  the left ventricular function of spontaneously  hypertensive rats.
abstract: OBJECTIVE
  To investigate whether the combination of exercise training with the angiotensin-converting enzyme inhibitor lisinopril will have an additional beneficial effect on left ventricular function in spontaneously hypertensive rats.
  
  
  METHODS
  Twelve-week-old male rats were assigned to treadmill running (Ht-Ex; 20 m/min at 5 degrees grade, 1 h/day, 5 days/week), or lisinopril treatment (Ht-Lis; 15 mg/kg per day by gavage), or treadmill running while treated with lisinopril (Ht-ExLis), and were compared with a sedentary group (Ht-Sed). Age-matched and sex-matched Wistar-Kyoto rats were controls.
  
  
  METHODS
  After 10 weeks of experimentation, left ventricular morphology and function were assessed from M-mode echocardiograms and transmitral Doppler spectra [early (E) and atrial peak velocities (A), their ratio (E/A), and E-wave deceleration time (Edec time) and slope (Edec slope)].
  
  
  RESULTS
  Ht-Sed exhibited prominent concentric left ventricular hypertrophy with systolic and diastolic dysfunctions evidenced by a significantly reduced fractional shortening (%FS) and 'pseudonormalization' of left ventricular filling, characterized by an apparently normal E/A ratio despite an underlying left ventricular relaxation abnormality. Exercise training did not significantly alter left ventricular morphology or function. Lisinopril alone attenuated left ventricular hypertrophy and enhanced diastolic function but had no significant effect on systolic function. Combining exercise training with lisinopril treatment increased %FS by 25%, decreased the E/A ratio and Edec slope by 35% and 37%, respectively, and increased Edec time by 82%.
  
  
  CONCLUSIONS
  Our results provide experimental evidence that lisinopril administration, when combined with moderate exercise training, is more promising in attenuating cardiac dysfunction than either agent alone in hypertension of a genetic origin.
authors.affiliation: Department of Physiology, College of Medicine and Health Sciences, Sultan Qaboos University, Al Khod, Muscat, Sultanate of Oman. ziada@squ.edu.om
authors.forename: Amal M
authors.initials: AM
authors.lastname: Ziada
mesh_terms: D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D003131:Combined Modality Therapy; D006973:Hypertension / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology / Q000628:therapy*; D017379:Hypertrophy, Left Ventricular / Q000188:drug therapy / Q000473:pathology / Q000628:therapy; D017706:Lisinopril / Q000627:therapeutic use; D008297:Male; D010805:Physical Conditioning, Animal; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D018487:Ventricular Dysfunction, Left / Q000188:drug therapy* / Q000503:physiopathology / Q000628:therapy*
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D017706:Lisinopril