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
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.