To test whether hypertension can cause hyperinsulinemia or insulin resistance, we performed intravenous glucose tolerance tests at 1 month and euglycemic clamps at 3 months after induction of two-kidney, one clip renovascular hypertension in rats. At 1 month, systolic pressure was higher in 21 clipped than in 12 control animals (161 ±5 mm Hg, range 134-187 mm Hg versus 119±3 mm Hg, range 108-146 mm Hg;p<0.001). Glucose tolerance, assessed as the glucose fractional disappearance rate between 3

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... d 11 minutes after the glucose injection, was similar in the clipped and sham groups (0.059±0.002 versus 0.056±0.002 min" 1 , respectively,p>0.4). The total area under the insulin curve during glucose tolerance tests was also similar in the clipped and sham groups (926 ±95 versus 869 ±126 microunits/mlxmin; p>0.4). There was no significant relation between systolic blood pressure and insulin area during glucose tolerance tests in the clipped group, but there was a positive rectilinear relation in the control group (r=0.66;p=0.01). Fourteen animals had euglycemic clamps 2 months after glucose tolerance tests. At that time, systolic pressure (direct femoral measurement) was higher in the seven clipped animals (189±13 mm Hg versus 122±5 mm Hg in controls; p<0.001). Insulin infusions of 1 and 4 milliunits/min/kg body wt effected similar plasma insulin levels in the two groups. Glucose requirements during 1 milliunit/min/kg insulin were higher in the clipped than the control group (6.1 ±0.7 versus 2.4±0.6 mg/min/kg, respectively; p<0.001). Glucose requirements during 4 milliunits/min/kg insulin were similar in the two groups (28.4±1.1 versus 26.8±2.8 mg/min/kg; p>0.5). Our data indicate that neither mechanisms leading to renovascular hypertension nor elevated blood pressure per se caused sustained hyperinsulinemia or insulin resistance in this rat model. (Hypertension 1991;18:341-347) H ypertension is associated with insulin resistance and hyperinsulinemia in lean and obese people. 1 " 11 Whether these abnormalities of carbohydrate metabolism and blood pressure are causally related is currently unknown. Based on effects of acute hyperinsulinemia to reduce renal sodium excretion 12 -14 and increase circulating catecholamine levels, 15 " 17 it has been proposed that hyperinsulinemia may contribute to the genesis or maintenance of hypertension in some patients. That proposal is supported by studies of weight loss 18 and physical training, 19 since blood pressure tends to fall in association with reduced insulin levels in both