Inhibition of Angiotensin Converting Enzyme (ACE) in Salt Receiving Fat-Fed Rats is Associated with Decreased Renal Oxidative Stress and Restoration of Neuronal Nitric Oxide Expression | ||
| Bulletin of Egyptian Society for Physiological Sciences | ||
| Article 26, Volume 27, Issue 1, June 2007, Pages 403-424 PDF (255.51 K) | ||
| Document Type: Original Article | ||
| DOI: 10.21608/besps.2007.37181 | ||
| Authors | ||
| Olfat Shaker* ; Samah El Attar; Laila El Said; Sandra Younan; Mary Youssef | ||
| Departments of Medical Biochemistry and Physiology, Faculty of Medicine, Cairo University. | ||
| Abstract | ||
| Impaired renal sodium excretion has been observed in fat induced obesity and was claimed to be multifactorial. Interestingly the subsequently developed hypertension can respond to one drug treatment, the angiotensin-converting enzyme inhibitor (ACE-I), suggesting a relationship between different causes of such impaired renal sodium excretion. This study aimed to elucidate such relationship and included six groups; group 1: rats fed the standard chow, group 2: moderately high fat diet (MHFD) fed rats, group 3: high salt fed (HSD) rats (4% Nacl for 1 week), group 4: MHFD+HSD, group 5: HSD+ACE-I and group 6: MHFD+HSD+ACE-I. It was found that 10 weeks of MHFD significantly increased the obesity index in groups 2, 4 and 6 compared to groups 1, 3 and 5 respectively and the systolic blood pressure in response to HSD in group 4 compared to group 3. Moreover MHFD led to significant albuminuria with significant reduction in urinary sodium excretion. Also MHFD increased significantly the renal malondialdehyde level (MDA) as an index of oxidative stress and angiotensinogen (AG) gene expression with significant decrease in urinary nitrites excretion and renal neuronal nitric oxide synthase (nNOS) expression in group 2 compared to group 1 and in group 4 compared to group 3. While HSD for one week did not have an impact on these previous parameters as evident by their non-significant differences between groups 3 and 1 and between groups 4 and 2. However, ACE inhibition in group 6 decreased significantly its urine albumin content, renal AG and MDA and significantly increased its urinary Na and nitrites excretion as well as its renal nNOS compared to group 4. Also ACE-I improved renal AG and nNOS in group 6 to be insignificantly different from those of group 5. These previous results suggest that a link coexist between renal angiotensinogen upregulation and renal oxidative stress mediated decrease in NO availability. In conclusion the MHF fed rats exhibited salt sensitivity accompanied by upregulation of renal angiotensinogen expression, increased oxidative stress and decreased nNOS expression, all of which could contribute to salt retention and hypertension. | ||
| Keywords | ||
| nNOS; sodium excretion; Oxidative Stress | ||
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