Effect of aliskiren, telmisartan and torsemide on cardiac dysfunction in l-nitro arginine methyl ester (l-NAME) induced hypertension in rats

Abstract

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.

Cardiac myeloperoxidase activity is elevated in hypertensive pregnant rats

“…Curiously, this trend of a lower heart rate occurred concomitantly with a significant increase in systolic blood pressure, suggesting a failed compensatory response. In accordance, previous studies reported that L-NAME induced an increase in systolic blood pressure and a diminished heart rate [29,30] .…”

“…To our knowledge, this is the first study showing that the cardiac MPO activity was increased in hypertension in pregnancy, which is in accordance with previous studies reporting elevations of circulating MPO levels in patients with preeclampsia [11,29] , suggesting that the most probable source of MPO is activated inflammatory cells in both heart (left ventricle) and circulation. Some study also supports this suggestion.…”

Mechanisms underlying the cardiac antifibrotic effects of losartan metabolites

“…In this regard, the TGF-β 1 -independent upregulation of CTGF and collagen synthesis induced by angiotensin II has been reported in different in vivo models of renal damage 39 , and in atrial fibrillation 40 . In addition, other mechanisms besides TGF-β 1 , and related to the renin-angiotensin system, hemodynamic stress 41 or inflammation/oxidative stress 17 , have been reported as inductors of myocardial fibrosis in L-NAME-treated rats. On the other hand, the mild antifibrotic effect shown by EXP3174 may be due to abrogation of chronic hemodynamic stress, independently of CTGF.…”

Beneficial Effects of Paeoniflorin Enriched Extract on Blood Pressure Variability and Target Organ Damage in Spontaneously Hypertensive Rats

“…), renovascular hypertensive animal models (2-kidney-1-clip, 2K1C [ 53 ] and 2-kidney-2-clip, 2K2C [ 54 ], etc. ), drug-induced hypertensive animal models (angiotensin-induced hypertension [ 55 ], L-nitro arginine methyl ester induced hypertension [ 56 ], etc. ), metabolic hypertensive animal models (excessive alcohol intake and high fat diet induced hypertensive rats [ 16 ], high-purine diet induced hypertensive rats [ 57 ], high-glucose/fat diet induced hypertensive rats [ 58 ], etc.…”