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.