Superoxide Dismutase Mimetic Tempol Normalized the Blood Pressure and Renal Functions in L-NAME Induced Hypertension Rats: The Role of Oxidative Stress

2013 
Increased oxidative stress has been suggested to be responsible for the development of hypertension and antioxidants are potentially useful therapeutic alternative for this disease. This study was performed to examine the role of superoxide dismutase mimetic-Tempol on hypertension and renal vasoconstriction induced by L-NAME administration. In addition, the participation of α1adrenoceptors and angiotensin II type I receptors have also been investigated. 32 male Sprague-Dawley rats were randomly assigned into four different groups (n=8 per group) to receive no treatment, Tempol treated, L-NAME treated and Tempol+L-NAME treated respectively for 21 days. Non-invasive blood pressure, renal functional parameters, acute renal haemodynamics, oxidative stress markers and histology studies were performed during the course of experimental period. L-NAME treatment induced hypertension, renal dysfunction and oxidative stress which were characterized by an increase of systolic blood pressure, impaired renal functional parameters, elevated plasma malondialdehyde levels and attenuated sensitivity to exogenous infused α1adrenergic agonists and Angiotensin II. Co-administration of Tempol+L-NAME completely abolished the abnormalities created by LNAME which can be proven by the decreased of systolic blood pressure, improved renal functional parameters with an enhancement of antioxidant enzymes. Moreover, the magnitude of renal cortical vasoconstrictions to exogenous infused α1adrenergic agonists and Angiotensin II has also been ameliorated. The available data suggested that the antioxidative stress activities required the interaction or crosstalk between SOD and NO. Nevertheless, SOD enzyme is the primary O2 - scavenger compared to NO under the NOS inhibited condition.
    • Correction
    • Source
    • Cite
    • Save
    • Machine Reading By IdeaReader
    37
    References
    0
    Citations
    NaN
    KQI
    []