NOCTURNAL BLOOD-PRESSURE ELEVATION IS RELATED TO ADRENOMEDULLARY HYPERACTIVITY, BUT NOT TO HYPERINSULINEMIA, IN NONOBESE NORMOALBUMINURIC TYPE-1 DIABETES

We tested the hypothesis that insulin is an independent risk factor fo r elevated blood pressure. As our model we selected type 1 diabetes wi th peripheral circulatory hyperinsulinemia induced by sc insulin treat ment. In 15 nonobese normoalbuminuric patients with type 1 diabetes (2 3.7 +/- 0.8 yr old) and in 15 healthy controls matched for age, sex, a nd body weight, ambulatory blood pressure was recorded over 24 h. The areas under the curve of free insulin (605 +/- 135 vs. 275 +/- 35 pmol /L . h; P = 0.03) and basal plasma epinephrine concentrations were hig her (170 +/- 10 vs. 130 +/- 10 pmol/L; P = 0.02), and the basal aldost erone level was lower (220 +/- 40 vs. 410 +/- 50 pmol/L; P = 0.009) in the patients. The nocturnal decline in systolic blood pressure was le ss pronounced (13 +/- 1 vs. 19 +/- 2 mm Hg; P = 0.007) in the patients . Multivariate adjustment (r(2) = 0.75; P = 0.0002) showed an effect o f basal plasma epinephrine and norepinephrine levels and body mass ind ex on the mean nocturnal systolic blood pressure, but showed no effect of age, sex, hemoglobin A(1c), aldosterone, or, in particular, insuli n. We found a blunted nocturnal fall in blood pressure in nonobese, no rmoalbuminuric type 1 diabetic patients. These patients showed increas ed adrenomedullary activity, and this predominantly contributed to the blood pressure alterations. We also found hyperinsulinemia in these p atients, but, after controlling for covariates, blood pressure was ind ependent of the insulin level.