Key result
Telmisartan leads antihypertensives in reducing L-NAME-induced cardiac fibrosis by ~87%.
Why the study?
Do aliskiren, telmisartan, and torsemide attenuate hypertension, nitric oxide depletion, collagen type I and III gene expression, and cardiac fibrosis in rats with L-NAME-induced hypertension?
Do aliskiren, telmisartan, and torsemide attenuate hypertension, nitric oxide depletion, collagen type I and III gene expression, and cardiac fibrosis in rats with L-NAME-induced hypertension?
In an L-NAME-induced hypertensive rat model, aliskiren, telmisartan, and torsemide all lowered blood pressure and restored nitric oxide levels, with telmisartan and torsemide demonstrating superior inhibition of cardiac fibrosis (87% and 85%) compared to aliskiren (40%).
Answers are grounded in this paper and cite their sources.
Hypothesis-generating in L-NAME rat model; leaves open clinical translation for fibrosis prevention.
Comparative study of cardio protective effect of aliskiren, telmisartan, and torsemide was carried out on l-nitro arginine methyl ester (l-NAME) induced hypertension in rats. The three drugs were given daily for 8 weeks simultaneously with l-NAME, with a control group for each drug and l-NAME. The degree of protection was assessed by measurement of systolic blood pressure and heart rate of animals every two weeks. At the end of the experimental period blood sampling was carried out for estimation of the level of NO2 (-)/NO3 (-). After which animals were sacrificed for heart dissection to detect collagen types I and III gene expression. Histopathological study was done to evaluate the extension of collagen deposits. The study revealed that the three drugs decreased blood pressure significantly compared to l-NAME. There was no significant difference between aliskiren and telmisartan in all measurements, but there was significant decrease in measurements of both aliskiren and telmisartan treated groups compared to torsemide starting from 4th week. There were insignificant changes in pulse rate values between the three l-NAME treated groups through the experiment. The three drugs significantly increased NO compared to l-NAME. Collagen I and III gene expression was significantly decreased by the three drugs but the highest percentage of inhibition was with telmisartan compared to l-NAME. Comparing the percentage inhibition of cardiac fibrosis, there was insignificant difference between telmisartan and torsemide treated groups while both were superior to aliskiren. In conclusion, further experimental studies are required to elucidate the potential cardioprotective mechanisms of aliskiren, telmisartan and torsemide, and assess their efficacy in treatment of heart failure.
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Sadek et al. (2014) studied L-NAME-induced hypertension and cardiac dysfunction in rats (n=48). Aliskiren, telmisartan, or torsemide vs. L-NAME (50 mg/kg/day) control and normotensive distilled water/drug controls was evaluated on Interstitial cardiac fibrosis (collagen volume fraction % and percentage inhibition vs L-NAME at 8 weeks) (p=<0.05). Telmisartan, torsemide, and aliskiren significantly reduced blood pressure and inhibited L-NAME-induced cardiac fibrosis by 87%, 85%, and 40%, respectively (p<0.05).
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