title: Long-term exercise training and angiotensin-converting enzyme inhibition differentially enhance myocardial capillarization in the spontaneously hypertensive rat.
abstract: OBJECTIVE
  To investigate whether combined treatment with lisinopril, an angiotensin-converting enzyme (ACE) inhibitor and exercise training would have an additive effect in enhancing the capillary supply of the left ventricular (LV) myocardium in spontaneously hypertensive rats (SHR).
  
  
  METHODS
  Twelve-week-old male SHR were divided into four groups (10-12 each): sedentary, sedentary treated with lisinopril (15-20 mg/kg per day by gavage), exercise trained, and exercise trained while treated with lisinopril. Exercise training consisted of 1 h a day/5 days a week of running on a treadmill.
  
  
  METHODS
  After 10 weeks of experimental protocols, capillary surface density and length density were sterologically determined in 1 mum thick LV tissue samples from perfuse-fixed hearts.
  
  
  RESULTS
  Lisinopril significantly reduced systolic blood pressure (SBP) and LV mass in the sedentary with lisinopril and exercise trained with lisinopril groups but did not affect the heart rate (HR). Exercise training did not reduce SBP or LV mass, but significantly reduced HR in the exercise trained and exercise trained with lisinopril groups. Lisinopril treatment (sedentary with lisinopril), exercise training (exercise) and their combination (exercise trained with lisinopril) significantly increased myocardial capillary surface area density by 26, 38 and 65% and length density by 38, 48 and 67%, respectively.
  
  
  CONCLUSIONS
  Lisinopril administration and exercise training independently enhanced myocardial capillarization through a reduction of myocardial mass and stimulation of angiogenesis, respectively. A combination of the two treatments enhanced myocardial capillarization more than either intervention alone. This may aid in the restoration of the normal nutritional status of cardiac myocytes compromised by the hypertrophic state of hypertension.
authors.affiliation: Department of Physiology, College of Medicine, Sultan Qaboos University, Muscat, Sultanate of Oman. ziada@squ.edu.om
authors.forename: Amal M
authors.initials: AM
authors.lastname: Ziada
authors.forename: Mohammed O
authors.initials: MO
authors.lastname: Hassan
authors.forename: Khurram I
authors.initials: KI
authors.lastname: Tahlilkar
authors.forename: Ibrahim M
authors.initials: IM
authors.lastname: Inuwa
mesh_terms: D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology*; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D002196:Capillaries / Q000187:drug effects / Q000502:physiology; D003131:Combined Modality Therapy; D003326:Coronary Circulation / Q000187:drug effects* / Q000502:physiology; D006339:Heart Rate / Q000187:drug effects; D006973:Hypertension / Q000188:drug therapy* / Q000503:physiopathology; D017379:Hypertrophy, Left Ventricular / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology; D017706:Lisinopril / Q000494:pharmacology*; D008297:Male; D010805:Physical Conditioning, Animal; D005082:Physical Exertion; D051381:Rats; D011918:Rats, Inbred SHR
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D017706:Lisinopril