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Published on: December 2, 2016
Left and right coronary circulation in left ventricular hypertrophy: effects of angiotensin converting enzyme
Yasuyuki Shimada1, Metin Avkiran
1Department of Cardiovascular Surgery, Kyoto Prefectural University of Medicine, Japan. yasuyuki.shimada@ma8.seikyou.ne.jp
Insights
Angiotensin converting enzyme (ACE) inhibitors like ramipril can improve coronary circulation in rats with left ventricular hypertrophy by lowering blood pressure. However, they did not reduce heart muscle enlargement or affect left coronary flow.
Area of Science:
- Cardiovascular Physiology
- Pharmacology
Background:
- Left ventricular (LV) hypertrophy, often caused by pressure overload, can impair coronary circulation.
- Understanding the effects of interventions on coronary blood flow in this condition is crucial.
Purpose of the Study:
- To investigate the impact of ramipril, an ACE inhibitor, on coronary circulation in a rat model of pressure overload-induced LV hypertrophy.
- To determine if ramipril affects coronary vascular resistance in the left and right coronary beds.
Main Methods:
- Rats underwent abdominal aortic constriction or sham surgery.
- Rams were treated with vehicle or varying doses of ramipril.
- Blood pressure, LV weight, and minimum coronary vascular resistance (MCVR/g) were measured.
Main Results:
- Aortic constriction increased blood pressure, LV weight, and bilateral MCVR/g.
- Ramipril dose-dependently reduced blood pressure and improved right coronary circulation.
- Ramipril did not alter LV mass or left coronary vascular resistance.
Conclusions:
- Both coronary hypertension and myocardial hypertrophy contribute to impaired coronary circulation in LV hypertrophy.
- ACE inhibitors may benefit coronary circulation in LV hypertrophy at appropriate doses.
Abstract:
The circulation in the left and right coronary beds in pressure overload-induced left ventricular (LV) hypertrophy was studied in Wistar male rats (n=6/group) that were subjected to abdominal aortic constriction or to sham-operation. From 3 to 6 weeks after surgery, the animals with aortic constriction received vehicle or 0.01, 0.1, or 1 mg/kg per day po of the angiotensin converting enzyme (ACE) inhibitor, ramipril. At 6 weeks, after measuring blood pressure in the carotid artery in vivo, the hearts were isolated and the left and right coronary beds subjected to independent perfusion. Minimum coronary vascular resistance per unit heart weight (MCVR/g) was determined in both beds during simultaneous infusion of 10 micromol/L adenosine. Aortic constriction resulted in a significant increase in blood pressure, LV weight/body weight ratio, and bilateral MCVR/g. Ramipril lowered arterial pressure in a dose-dependent manner and reversed the increased right MCVR/g at the anti-hypertensive dose, but it did not affect LV mass or left MCVR/g. These results suggest that both coronary hypertension and myocardial hypertrophy contribute to the global impairment of coronary circulation in LV hypertrophy. ACE inhibitors may improve coronary circulation in LV hypertrophy when administrated at an appropriate dose and for a sufficient period.
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