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Vitamin C and quinapril abrogate LVH and endothelial dysfunction in aortic-banded guinea pigs
1Department of Pharmacology, Therapeutics, and Toxicology and Sir Geraint Evans Wales Heart Research Institute, University of Wales College of Medicine, Heath Park, Cardiff CF14 4XN, United Kingdom.
Insights
Left ventricular hypertrophy (LVH) is a cardiovascular risk factor. Treatments targeting oxidative stress and improving endothelial function, like quinapril and vitamin C, can inhibit LVH development.
Area of Science:
- Cardiovascular Research
- Endothelial Biology
- Pharmacology
Background:
- Left ventricular hypertrophy (LVH) is a significant cardiovascular risk factor.
- Endothelial dysfunction may play a role in the development of LVH.
- Aortic banding in guinea pigs creates a model for pressure overload-induced LVH.
Purpose of the Study:
- To investigate the role of endothelial dysfunction in LVH.
- To evaluate the effects of quinapril and vitamin C on LVH and associated markers.
Main Methods:
- Induced LVH in Dunkin-Hartley guinea pigs via aortic banding.
- Measured blood pressure, cardiac hypertrophy markers, and plasma levels of ANG II, ET-1, and TNF-alpha.
- Assessed coronary microvascular endothelial cell (CMEC) superoxide production and cGMP levels.
- Treated animals with quinapril and/or vitamin C.
Main Results:
- Aortic banding increased blood pressure, heart-to-body weight ratio, ANG II, ET-1, TNF-alpha, and CMEC superoxide production, while decreasing cGMP levels.
- Quinapril and vitamin C treatment inhibited increases in heart-to-body weight ratio, ANG II, ET-1, TNF-alpha, and superoxide production.
- Treatments restored CMEC cGMP responses to normal levels without affecting blood pressure.
Conclusions:
- Quinapril and vitamin C inhibit LVH development caused by pressure overload.
- These effects are mediated by reducing oxidative stress and improving endothelial function.
- Increased nitric oxide bioavailability is a key mechanism in the observed benefits.
Abstract:
Left ventricular hypertrophy (LVH) is a cardiovascular risk factor. A possible role for endothelial dysfunction in this condition was investigated in a Dunkin-Hartley guinea pig aortic-banded pressure overload-induced model of LVH. Aortic banding produced significant elevation of fore- and hindlimb blood pressure (BP), heart-to-body weight ratios, plasma angiotensin II (ANG II), endothelin-1 (ET-1), tumor necrosis factor-alpha (TNF-alpha) levels, and coronary microvascular endothelial cell (CMEC) NAD(P)H-dependent superoxide (O) production, and a significant decrease in basal and stimulated CMEC cGMP levels. Treatment of aortic-banded animals with the angiotensin-converting enzyme inhibitor quinapril and the antioxidant vitamin C, either alone or in combination, did not affect BP but caused a significant inhibition of the increases in the heart-to-body weight ratio, ANG II, ET-1, and TNF-alpha levels, and O production and restored cGMP responses to levels comparable with sham-operated animals. These data suggest that quinapril and vitamin C are capable of inhibiting LVH development due to pressure overload via mechanisms that involve the inhibition of oxidative stress, an improvement in coronary endothelial function, and increased nitric oxide bioavailability.
