Hypertension is a very common cardiovascular disease which carries a risk of many complications affecting the cardiovascular system and other systems of the body, so proper drug choice for treatment of hypertension is necessary not only to normalize the blood pressure but also to protect against its cardiovascular complication such as left ventricle hypertrophy ,heart failure and coronary heart diseases.
Valsartan which is one of the angiotensin receptor blockers (ARBs) and amlodipine which a dihydropyridine calcium channel blocker (CCBs) are powerful antihypertensive drugs, the present study was carried out to study the possible cardio protective effect of these drugs in two different types of hypertension (high renin and low renin hypertension) by measuring the following parameters: systolic, diastolic and mean arterial blood pressure, cardiac weight to total body weight ratio, free left ventricular wall thickness, ST segment height and percent surface area of the infarct size using triphenyl tetrazolium chloride stain.
To study the cardioprotective effect of each drug 120 adult male albino rats were divided into 2 models according to renin level:
Model( I )high renin hypertension model which was divided into 5 groups, group (I) which was a normal control group ,group( II ) which was a vehicle group, group III was a non-treated high renin hypertensive group in which high renin hypertension was induced by unilateral renal artery ligation and was achieved 4 weeks after surgery, group IV was a valsartan treated group where valsartan was administrated (30 mg /kg/day) orally for 4 weeks, group V was amlodipine treated group where amlodipine was administrated (10 mg /kg /day) orally for 4 weeks. Model ( II) low renin hypertension model which was divided into 5 groups, group (I) which was a normal control group, group( II ) which was a vehicle group, group III was a non treated low renin hypertensive group in which low renin hypertension was induced by induced by DOCA and salt and was achieved 4-6 weeks from zero time of the experiment, group IV was a valsartan treated group where valsartan was administrated (30 mg /kg/day)orally for 4 weeks, group V was amlodipine treated group where amlodipine was administrated (10 mg /kg /day) orally for 4 weeks. Finally myocardial infarction was experimentally induced in all hypertensive rats by isoprenaline (S.C) injection in the abdominal region.
This study revealed that valsartan was effective antihypertensive drug in high renin hypertension only while it was not effective in trearment of low renin hypertension.
Valsartan was proved in this study to decrease left ventricle hypertrophy in high renin hypertension and in low renin hypertension.
Also valsartan administration as an antihypertensive drug in high renin hypertension resulted in decreasing coronary ischemia found with this type of hypertension and even after myocardial infarction induction valsartan was effective as it decreases the elevated ST segment and the percent surface area of infarct size.
Valsartan administration in low renin hypertension failed to decrease coronary ischemia found with this type of hypertension before experimental myocardial infarction induction, while after induction of myocardial infarction by S.C injection of isoprenaline, valsartan produced a significant decrease in ST segment height and in percent surface area of infarct size, this occurred as with myocardial infarction there is activation of renin angiotensin system which proves that valsartan had a cardioprotective effect when the renin angiotensin system is stimulated and could be used in postmyocardial infarction.
This study revealed that amlodipine was an effective hypotensive drug in both high renin and low renin hypertension.
Amlodipine in this study succeeded to decrease left ventricle hypertrophy in high renin as well as in low renin hypertension
Amlodipine administration as a hypotensive drug in high renin as well as in low renin hypertension produced an improvement in myocardial ischemia resulted from both types of hypertension and this effect remains after experimental induction of myocardial infarction
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