Effect of angiotensin II receptor antagonism on vascular hypertrophy and aortic impedance in abdominal aortic-banded rat

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.