| Objective: Setback in insulin resistance (IR) has been described in patients with essential hypertension and animal model. Angiotensin II plays a central role in the regulation of systemic arterial pressure through its systemic synthesis via the renin-angiotensin-aldosterone cascade. The mechanism of the relationship between insulin resistance and renin-angiotensin-aldosteron system (RAAS) in hypertension is unclear. The study is to evaluate relationship between RAAS and IR and effects of losartan (angiotensin AT (1) receptor antagonists) therapy on activity of RAAS and insulin resistance in fructose-fed SHR (spontaneously hypertensive rats).Methods: Ten-week-old SHR was randomly divided into there groups (control group, fructose group and losartan group). Control group were placed on breeder's chow and fructose group on a 60% fructose diet; losartan group were placed on a 60% fructose diet and losartan. Measurements of fasting glucose, insulin in the blood was made. The examination also included plasma glucose and insulin levels during oral glucose tolerance test (OGTT) (0, 30, 60, 120,180min) ,blood pressure, body weight, renin, aldosteron, angiotensin II at end of 8 weeks after treatment.Results: 1. The change in body weight was not difference in three groups at the end of 8 weeks after treatment. 2. At the end of 8 weeks after treatment, Fructose-fed were higher systolic blood pressure (SBP) animals than control group (224.80±3.01 vs. 207.78±12.51mmHg, P<0.01); this increase in SBP was prevented by losartan treatment (184.2±15.57 vs. 224.80±3.01 mmHg, P<0.001). 3. Fasting blood glucose (FBG) concentration (6.06±1.09, 5.87±1.57and 5.6±0.52 mmol Liter"1, P>0.05) was not difference in three groups. But 30min(14.43±2.68 vs. 9.48±2.54 mmol-Liter'1, P<0.001), 60min(12.48±1.09 vs. 8.41±0.45 mmol-Liter'1, P<0.001), 120min(l 1.72±3.00 vs. 7.98±1.40 mmol-Liter'1, P<0.01) and area of glucose (P<0.001) were higher than control group's in the blood. Fasting insulin (FINS) (60.06±32.45 vs. 33.15±7.86 u U.ml-1, P<0.01), 60min(68.76±13.68 vs. 32.66±10.52 y U.ml"1, P<0.001) insulin concentration logarithm and area of insulin (PO.001) logarithm in the blood were high compared with controls, ISI were low in fructose group (-5.80±0.61 vs. -5.29±0.32,) (P<0.05). but those was improve in losartan group (P<0.05). 4. Angiotensin II (748.01 ±207.98 vs. 176.97±81.28 pg.ml"1, P<0.05) and Aldosterone (102.2±17.87 vs. 65.56±17.61 pg.ml-1, P<0.01) in fructose-fed SFIR were high comparedwith those in control group, high Aldosterone were protected in losartan group (65.56±20.68 vs. 102.2±17.87 pg.ml"1, P<0.01). 5. There were no correlations between the change in rennin activity and any of insulin concentration logarithms in either fructose group or losatan group (P>0.05). In fructose group, It have shown correlations between Angiotensin II and fasting, 60min insulin concentration, area of insulin logarithm; Aldosterone was related to 60min insulin concentration and area of insulin logarithm (P<0.005); While SBP was related to fasting, 60min insulin concentration logarithm , aldosterone and angiotensin II (P<0.005). By regression study it was found that angiotensinII and area of insulin logarithm regression coefficient (B) was 617.05, Beta was 0.626, t was 3.109 and P was 0.007; Aldosterone and 60min insulin concentration logarithm regression coefficient (B) was 38.695, Beta was 0.668, / was 3.476 and P was 0.003. In losartan group, there was significant correlation with aldosterone and 60 min insulin concentration logarithm(P<0.01), ISI(r=-0.562, P=0.002); Controlling angiotensin II, Aldosterone was related to 60 min insulin concentration logarithm and ISI(r=0.562 , P=0.004 and r=-0.50, P=0.003 ). If controlling angiotensinII and Aldosterone, SBP would be related to fasting insulin concentration and area of insulin logarithm(r=0.459 , P=O.Q24 and r=0.506, P=0.012). By regression study it was found that aldosterone and 60min insulin concentration...
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