Abstract
Hypertension is a serious problem that is recently thought to be associated with damaging effects on target organs partially via oxidative stress. On the other hand, there is accumulating literature describing some sort of therapeutic interaction between antioxidant enzymes in vital organs and hypertension. Therefore, the aim of this study is to investigate the possible effect of a direct renin inhibitor, aliskiren, used in treatment of hypertension via renin-angiotensin-aldosterone system (RAAS), on selected anti-oxidant enzymes in hepatic homogenates in DOCA salt-induced hypertesnive albino rats. Thirty male wister albino rats were assigned randomly into 3 groups (n = 10/ group). Group 1 received no treatement and serves as control. Group 2 received 0.5% carboxymethylcellulose sodium ip as a solvent of aliskiren, as a direct renin inhibitor (DRI). Group 3 received aliskiren 100 mg/kg/day ip for 4 weeks through gastric tube. Systolic blood pressure (SBP) was measured every week and its mean was recorded at the end of the study. Superoxide dismutase (SOD) enzyme in RBCs lysates, activities of catalase (CAT) and glutathione peroxidase enzymes and thiobarbituric acid reactive substance (TBARS), as a marker of lipid peroxidation, in hepatic homogenates were measured at the end of the study. DRI produced a marked reduction in mean SBP of hypertensive rats. It also significantly (p < 0.05) increased the activities of measured anti-oxidant enzymes while it significantly (p < 0.05) reduced TBARS in liver homogenates. These results indicated that renin possesses an oxidative effect in the liver in hypertensive rats. Aliskiren, in addition to its powerful anti-hypertensive effect, it could induce a great anti-oxidant effect in liver homogenates of DOCA salt-hypertensive rats.
Highlights
The renin angiotensin aldosterone system (RAAS) plays an important role in the regulation of blood pressure and body fluid volume. It stimulates the synthesis of angiotensin II (Ang II) via two main steps: production of angiotensin I from angiotensinogen via cleavage by renin enzyme to convert it to Ang II by angiotensin-converting enzyme (ACE)
This role could be related to the increase in blood pressure and aldosterone levels by Ang II and to its remodeling effects on cardiac, vascular and renal tissue that lead to end-organ damage [1]
The results revealed that ip daily dose for 4 weeks of the tested drug significantly reduced Systolic blood pressure (SBP), increased levels of Superoxide dismutase (SOD) enzyme in erythrocyte lysates, augmented the activity of CAT and Glutathione peroxidase (GPx) anti-oxidant enzymes and reduced thiobarbituric acid-reactive substance (TBARS), as a marker of lipid peroxidation, in liver homogenates of hypertensive rats
Summary
The renin angiotensin aldosterone system (RAAS) plays an important role in the regulation of blood pressure and body fluid volume. It stimulates the synthesis of angiotensin II (Ang II) via two main steps: production of angiotensin I from angiotensinogen via cleavage by renin enzyme to convert it to Ang II by angiotensin-converting enzyme (ACE). RAAS has an important role in the development of many pathological states This role could be related to the increase in blood pressure and aldosterone levels by Ang II and to its remodeling effects on cardiac, vascular and renal tissue that lead to end-organ damage [1]. T cells stimulate the release of cytokines that lead to vasoconstriction and sodium retention contributing to the development of hypertension [2]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
