CARDIAC-HYPERTROPHY IN DIABETIC SPONTANEOUSLY HYPERTENSIVE RATS - ROLE OF ANGIOTENSIN-II

Citation
Mj. Black et al., CARDIAC-HYPERTROPHY IN DIABETIC SPONTANEOUSLY HYPERTENSIVE RATS - ROLE OF ANGIOTENSIN-II, Clinical and experimental pharmacology and physiology, 24(6), 1997, pp. 445-448
Citations number
16
Categorie Soggetti
Pharmacology & Pharmacy",Physiology
ISSN journal
03051870
Volume
24
Issue
6
Year of publication
1997
Pages
445 - 448
Database
ISI
SICI code
0305-1870(1997)24:6<445:CIDSHR>2.0.ZU;2-N
Abstract
1. In the present study the role of angiotensin II (AngII) in the deve lopment of cardiac hypertrophy in diabetes combined with hypertension was investigated. 2. Diabetes was induced in 8-week-old male spontaneo usly hypertensive rats (SHR) by intravenous injection of streptozotoci n (45 mg/kg bodyweight), Diabetic SHR were treated with the angiotensi n-converting enzyme (ACE) inhibitor ramipril at a dose of 0.4 mg/kg pe r day. 3. Twelve weeks following the onset of diabetes, hearts were ar rested in diastole and were perfusion-fixed. The right ventricle and l eft ventricle plus septum were weighed and the volume of the ventricul ar walls was determined using the Cavalieri principle, 4. Induction of diabetes in SHR led to a significant reduction in bodyweight compared with non-diabetic control SHR and this was not affected by ramipril t reatment, The development of hypertension was not as great in diabetic SHR compared with controls, such that at 12 weeks following the onset of diabetes systolic blood pressures (SEP) averaged 191 +/- 3 and 230 +/- 4 mmHg in diabetic SHR and controls, respectively, Ramipril treat ment significantly lowered SEP in diabetic SHR, 5. The left ventricle plus septum volume:bodyweight ratio (LV vol:BW) was significantly high er in diabetic SHR compared with controls (3.83 +/- 0.19 and 3.26 +/- 0.16 mm(3)/g, respectively). Ramipril treatment did not affect growth of the left ventricle in diabetic SHR with the LV vol:BW ratio averagi ng 3.95 +/- 0.14 mm(3)/g, Similar trends on growth were observed in th e right ventricle,6. In conclusion, the development of cardiac hypertr ophy in diabetic SHR appears to occur by mechanisms independent of Ang II and the elevation of blood pressure.