M. Obayashi et al., Effect of angiotensin II receptor antagonism on vascular hypertrophy and aortic impedance in abdominal aortic-banded rat, AM J HYPERT, 12(4), 1999, pp. 381-387
Vascular hypertrophy is considered to be an adaptive response to increased
arterial wall stress in hypertension. Although there are several reports co
ncerning the effect of angiotensin II inhibition on the development of vasc
ular hypertrophy, little information is available as to its effect on vascu
lar hypertrophy in parallel with the evaluation of arterial wall characteri
stics. The goal of this study was to evaluate the effect of angiotensin II
type 1 receptor antagonist TCV-116 on pressure overload-induced vascular hy
pertrophy in parallel with the assessment of aortic impedance.
Low dose (LD; 0.3 mg/kg/day) or high dose (HD; 3.0 mg/kg/day) of TCV-116 wa
s administered to abdominal aortic-banded rats over 4 weeks; then hemodynam
ics and morphology were evaluated. In both the LD and HD groups, blood pres
sures were decreased to a similar extent compared with those of the vehicle
-treated group (P < .05). Left ventricular (LV) weight and LV weight/body w
eight ratio was inhibited in both TCV-116-treated groups (P < .05), whereas
the media cross-sectional area of the aorta was inhibited only in the HD g
roup (P < .05). After the treatment of TCV-116 (LD, HD), total systemic res
istance was decreased compared with the vehicle-treated group (P < .05), bu
t there was no significant difference between the TCV-116-treated groups. I
n contrast, the first harmonic of the impedance modulus revealed the decrea
se only in the HD group (P < .05).
TCV-116 attenuated the development of pressure overload LV hypertrophy and
vascular hypertrophy as well; however, the dose of TCV-116 required for the
inhibition of vascular hypertrophy was significantly higher than that for
LY hypertrophy. Vascular hypertrophy may be less pressure dependent than ca
rdiac hypertrophy. On chronic addition of high dose of TCV-116, arterial wa
ve reflection was decreased in association with the attenuation of vascular
hypertrophy. (C) 1999 American Journal of Hypertension, Ltd.