ROLE OF ANGIOTENSIN-II IN HIGH-FRUCTOSE INDUCED LEFT-VENTRICULAR HYPERTROPHY IN RATS

Recent studies suggest the linkage of hypertension and insulin resista nce. High fructose diet is known to induce hyperinsulinemia and hypert ension in rats. In a previous study, however, high fructose (66%) diet failed to elevate blood pressure but increased left ventricular weigh t in Sprague-Dawley rats. In the present study, we investigated the pr ecise mechanism of high fructose diet-induced changes in the cardiovas cular system in rats. Intake of fructose-enriched diet for 2 weeks inc reased serum insulin and plasma angiotensin II levels. Urinary excreti on of sodium and norepinephrine was not changed. Blood pressure measur ed directly through an indwelling catheter was not increased, but left ventricular weight and protein content were increased by high fructos e diet. To further elucidate the role of the renin-angiotensin system, an angiotensin II type I receptor antagonist, TCV-116, was given oral ly at 1 mg/kg per day with either normal or high fructose diet. Concom itant administration of TCV-116 did not affect plasma glucose or serum insulin levels. Plasma angiotensin II was increased, but neither urin ary sodium nor norepinephrine was changed by TCV-116. TCV-116 similarl y decreased blood pressure in rats on normal and high fructose diets. Increase in left ventricular weight induced by high fructose diet was prevented by the concomitant administration of TCV-116. On the other h and, left ventricular weight in control rats was not changed by TCV-11 6. In conclusion, increased plasma angiotensin II may account for the left ventricular hypertrophy induced by high fructose diet, whereas he modynamic change, sodium retention, and the sympathetic nervous system do not play an important role.