ACE-INHIBITION REDUCES LEFT-VENTRICULAR MASS-INDEPENDENT OF PRESSURE WITHOUT AFFECTING CORONARY FLOW AND FLOW RESERVE IN SPONTANEOUSLY HYPERTENSIVE RATS
K. Kaneko et al., ACE-INHIBITION REDUCES LEFT-VENTRICULAR MASS-INDEPENDENT OF PRESSURE WITHOUT AFFECTING CORONARY FLOW AND FLOW RESERVE IN SPONTANEOUSLY HYPERTENSIVE RATS, The American journal of the medical sciences, 314(1), 1997, pp. 21-27
Systemic and regional (including coronary) hemodynamics were studied i
n spontaneously hypertensive and normotensive Wistar Kyoto rats after
3 weeks of treatment with one of the three doses of the angiotensin co
nverting enzyme inhibitor, ramipril. The effects of respective treatme
nts on cardiovascular mass and systemic, coronary, and regional hemody
namics (at rest, during maximal treadmill exercise, and during dipyrid
amole infusion) then were evaluated in conscious rats using radiomicro
sphere techniques. Low-dose ramipril (10 mu g/kg/day by gavage) neithe
r decreased arterial pressure nor reduced cardiac mass. However, mediu
m (100 mu g/kg/day) and high (1 mg/kg/day) doses reduced total cardiac
and left ventricular masses to the same extent in spontaneously hyper
tensive rats, despite a much greater fall in arterial pressure with a
high dose. Resting cardiac index, and myocardial and all other organ b
lood hows remained unchanged in both strains. When compared with Wista
r Kyoto rats, coronary circulation was impaired in untreated spontaneo
usly hypertensive rats (ie, reduced coronary flow and flow reserve and
increased minimal coronary vascular resistance during dipyridamole in
fusion). This remained unchanged by ramipril. Furthermore, significant
(and comparable) increases in cardiac index and myocardial blood how
and decreases in coronary vascular resistance were produced by maximal
treadmill exercise in both strains. This also was unaffected by ramip
ril. These data showed that angiotensin converting enzyme inhibition w
ith suboptimal and optimal hypotensive doses of ramipril reversed left
ventricular hypertrophy in spontaneously hypertensive rats, but coron
ary how, flow reserve, and minimal coronary vascular resistance remain
ed unchanged despite left ventricular hypertrophy reversal.