Captopril modifies angiotensin-converting enzyme but not choline acetyltransferase gene expression in the frontal cortex of renovascular hypertensive rats
Journal Title: National Journal of Physiology, Pharmacy and Pharmacology - Year 2017, Vol 7, Issue 6
Abstract
Background: The classic renin-angiotensin system (RAS) has a role in the cardiovascular system and water homeostasis in the body, but recently, the existences of this system with all of its components including angiotensinogen, angiotensinconverting enzyme (ACE), and angiotensin receptors have been shown in the mammalian brain. Recent clinical studies suggest that treatment of hypertensive patients with the RAS affecting drugs, such as captopril improves their cognitive function. Aims and Objectives: This study was conducted to evaluate the effects of captopril on the frontal cortex levels of ACE and choline acetyltransferase (ChAT) in renovascular hypertensive rats receiving captopril. Materials and Methods: The rats were randomly divided into 3 groups of 8 animals; control, Goldblatt two kidney one clip (2K1C) hypertensive rats and Goldblatt 2K1C hypertensive rats received 5 mg/kg captopril. After 8 days of treatment; the rats were sacrificed and expression of ACE and ChAT in the frontal cortex were assessed by real-time polymerase chain reaction. The results were analyzed with two-way ANOVA test using SPSS software and the level of significance was set at P < 0.05. Results: Captopril treatment decreased the levels of ACE mRNA in the frontal cortex of renovascular hypertensive rats but has no significant effect in the ChAT mRNA levels. Conclusion: Captopril as a nootropic drug has no significant effect on the ChAT gene expression in the frontal cortex of renovascular hypertensive rats and it may exert its memory enhancing effect on the frontal cortex via a non-cholinergic mechanism.
Authors and Affiliations
Marzieh Vahid, Farzaneh Ganji, Hamid Sepehri, Zahra Nazari
Keywords
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- EP ID EP289867
- DOI 10.5455/njppp.2017.7.0202314022017
- Views 36
- Downloads 0
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