[The effect of insulin in primary hyperaldosteronism].

BACKGROUND

Deteriorated insulin resistance was described in patients with essential hypertension. The objective of the present study was to test at the receptor and postreceptor level the presence of insulin resistance in hypertension with primary hyperaldosteronism.

METHODS AND

RESULTS

The diagnosis of primary hyperaldosteronism was assessed by means of biochemical and imaging methods in 123 hypertensive patients with a normal glucose tolerance (mean age 49.8 +/- 12.9 years, range 20-65 years, BMI 28.3 +/- 4.8 kg/m2). The blood pressure was monitored for 24 hours by a Spacelab tonometer (systolic BP 168 +/- 21 mm Hg, diastolic BP 103 +/- 9 mm Hg, plasma aldosterone in a recumbent position 426 +/- 472 pg/ml (normal values under 150 pg/ml), concentration of serum potassium 3.6 +/- 0.6 mmol/l. The control group was formed by seven volunteers matched for age and BMI. The patients had a normal basal blood sugar level in the morning (5.0 +/- 0.6 mmol/l), the basal insulinaemia was 19.5 +/- 10.2 mU/l. The insulin resistance was examined using the method of an euglycaemic hyperinsulinaemic clamp on Biostator at an insulin infusion rate of 1 mU/kg/min. Concurrently insulin receptors on red blood cells were assessed. The plasma potassium concentration was maintained by means of insulin receptors on erythrocytes. The potassium plasma concentration was maintained by means of a linear dosage device with potassium at constant physiological levels (after previous supplementation). In patients with primary hyperaldosteronism the authors observed, as compared with healthy controls, a lower glucose consumption during the clamping (glucose disposal rate 18.7 +/- 4.8 vs 29.3 +/- 3.7 mumol/kg/min, p < 0.01), a rise of the metabolic glucose clearance (3.8 +/- 1.5 vs. 7.0 +/- 1.1 ml/kg/min, p < 0.01 and an index of tissue sensitivity for insulin) 23.7 +/- 9.8 vs. 37.5 +/- 11.6 mumol/kg/min per mU/l x 100, p < 0.02). The characteristics of insulin receptors in patients with primary hyperaldosteronism did not differ from normal values. No correlation was found between the plasma concentration of aldosterone and the index of tissue sensitivity for insulin (r = 0.011, NS).

CONCLUSIONS

It may be stated that primary hyperaldosteronism is associated with insulin resistance at the postreceptor level. Its pathogenesis has not been elucidated so far and will be the object of future research.