Diets containing 8%
salt or 4%
fructose (FR) cause
insulin resistance and increase tissue
methylglyoxal and
advanced glycation end products (AGEs), platelet cytosolic-free
calcium, and systolic blood pressure (SBP) in rats. In WKY rats, we have shown that moderately high
salt, 4% NaCl (MHS) alone in diet does not cause
hypertension, and when given along with 4% FR it does not have an additive effect.
N-acetylcysteine (NAC) or
L-arginine (ARG), treatment alone does not prevent
hypertension in this model. The objectives of this study were to investigate the effect of NAC plus ARG in diet on SBP, platelet cytosolic-free
calcium in a MHS + FR model, and to measure the plasma levels of
methylglyoxal and the AGE,
methylglyoxal-derived
hydroimidazolone (MGH). At 7 weeks of age, WKY rats were divided into three groups: control group was given regular rat chow (0.7% NaCl) and water; MHS + FR group, diet containing 4% NaCl and 4% FR in
drinking water; and MHS + FR + NAC + ARG group, MHS diet supplemented with 1.5%
N-acetylcysteine (NAC) and 1.5%
L-arginine (ARG), and 4% FR in
drinking water, and followed for 6 weeks. NAC + ARG prevented the increase in platelet cytosolic-free
calcium and SBP in MHS + FR treated rats. There was no difference in mean values of plasma
methylglyoxal and MGH among the groups. In conclusion, NAC + ARG treatment is effective in preventing
hypertension in a moderately high
salt + FR-induced animal model. Plasma
methylglyoxal and MGH may not represent tissue modification or, alternatively, other tissue AGEs, derived from
methylglyoxal or other
aldehydes, may be involved in
hypertension in this model.