A Moderately High Fat Diet Promotes Salt-Sensitive Hypertension in Obese Zucker Rats by Impairing Nitric Oxide Production

Abstract

The objective of this research was to examine the contribution of a moderately high fat (MHF) diet to the development of salt-sensitive hypertension in obese Zucker rats. Lean and obese Zucker rats were fed either a MHF diet or a diet of standard rat chow (control diet) for 10 weeks. From week 4 through week 10, the drinking water was supplemented with 1% NaCl. Blood pressure was measured weekly, and urinary excretion of nitric oxide metabolites (NO(x)) was determined at weeks 4 and 10. At week 10, renal nitric oxide synthase (NOS) activity was assessed in kidney homogenates. Blood pressures of obese, but not lean, rats on the MHF fat diet were significantly increased by salt-supplementation, whereas blood pressures of rats on the control diet were not appreciably affected. NO(x) excretion was increased in response to salt-supplementation in rats on the control diet, with the effect being particularly dramatic in obese rats. After salt-supplementation, NO(x) excretion by rats on the MHF diet was lower than rats on the control diet. In obese rats on the MHF diet, this decrease in NO production was accompanied by a reduction in renal NOS activity. These results indicate that obese rats are more inclined than lean rats to develop diet-induced hypertension in response to a moderately high fat, salt-supplemented diet. Furthermore, they suggest that MHF diet-induced defects in NO production may promote the salt-sensitivity of blood pressure in obese Zucker rats, which appear to require more NO to maintain blood pressure during a salt challenge.

Chronic AT2 receptor activation increases renal ACE2 activity, attenuates AT1 receptor function and blood pressure in obese Zucker rats

“…Obese rats excreted higher amount of total urinary nitrates/nitrites compared to lean rats. Consistent with previous studies, 36 excretion of urinary nitrates/nitrites, as measured on days 2 and 14 of the treatment period was greater in obese rats compared to lean rats. CGP-treatment had no effect on nitrates/nitrites excretion in lean rats but caused an increase in obese rats only during the initial (measured at 2 day) treatment period.…”

Effects of Angiotensin II AT1^|^ndash;Receptor Blockade on High Fat Diet^|^ndash;Induced Vascular Oxidative Stress and Endothelial Dysfunction in Dahl Salt-Sensitive Rats

“…Endothelial dysfunction significantly contributes to the development of HF-induced hypertension (3, 6). Several studies have indicated that a HF diet induces endothelial dysfunction through the generation of oxidative stress (9, 10).…”

“…Salt restriction decreased blood pressure in obese subjects more significantly than in non-obese subjects, and subjects that undergo weight loss demonstrated a suppression in salt-induced blood pressure increases (2). In rats, long treatment with a high fat (HF) diet caused greater salt-induced increases in blood pressure (3 – 5). It has also been demonstrated that endothelial dysfunction closely contributes to the development of HF diet–induced hypertension (6 – 8).…”

Protective effect of Garcinia against renal oxidative stress and biomarkers induced by high fat and sucrose diet

“…Rats fed HFD, resulted in decrease in serum and renal NO production (Table 3), indicating that obese rats are more liable to develop hypertension. Furthermore, HFD -induced defects in NO production may promote the salt-sensitivity of blood pressure, which appears to require more NO to maintain blood pressure during a salt challenge [50]. …”