Carbohydrate enriched diets have been shown to elevate blood pressure
in the rat. The precise mechanism by which carbohydrate feeding elevat
es blood pressure is not known. We evaluated the role of the renin-ang
iotensin system in the etiology of fructose-induced hypertension. Losa
rtan potassium, an angiotensin II (ATI) Type 1 (AT(1)) receptor antago
nist, was utilized to assess the blood pressure response to fructose t
reatment. Male Sprague-Dawley rats were divided into 3 groups. Rats in
the control group were fed regular chow. The other two groups were fe
d 60% fructose diet for 4 weeks. One of these groups was chronically t
reated with losartan potassium in drinking water. Throughout the study
there was no significant difference in body weight between the three
groups. There was a significant increase in blood pressure of fructose
-treated rats within one week of treatment which remained elevated for
the remainder of the study. Chronic losartan treatment significantly
attenuated the rise in blood pressure. Within two weeks both the dipso
genic response and the presser response to AII demonstrated complete b
lockage of AII receptors. These results suggest that the renin-angiote
nsin; system plays a role in the development of fructose-induced hyper
tension.