Serum aldosterone changes during hyperinsulinemia are correlated to body mass index and insulin sensitivity in patients with essential hypertension

Objective To measure the effects of hyperinsulinemia on serum electrolyte s tatus and associated hormones, and on serum free fatty acid (FFA) concentra tions, in patients with essential hypertension. Design and methods The serum electrolyte status (Na, K, Ca, ionized Ca, Mg, P, pH) and associated hormones [plasma renin activity (PRA), serum parathy roid hormone (PTH) and aldosterone concentrations], and FFA were measured d uring an euglycemic hyperinsulinemic clamp test in 49 patients with untreat ed essential hypertension. Results Serum potassium, phosphate, PTH, and FFA concentrations decreased d uring hyperinsulinemia, while serum ionized calcium concentration, pH, and PRA increased significantly (P < 0.05). The changes in serum potassium and magnesium were both inversely related to the insulin-mediated glucose uptak e (r = -0.62, P < 0.0001; r = -0.31, P < 0.05, respectively). Both body mas s index (BMI) and insulin-mediated glucose disposal were significantly corr elated to the changes in serum aldosterone concentration during hyperinsuli nemia (r = 0.41, P < 0.01; r = -0.40, P < 0.01, respectively). The change i n serum aldosterone during the clamp test was not significantly related to the change in PRA, but tended to correlate to the change in potassium conce ntration (r = 0.25, P = 0.10). A less pronounced reduction in FFA during in duced hyperinsulinemia was associated with low insulin sensitivity(r = -0.3 5, P < 0.05). Conclusion Hypertensive patients with normal BMI and a more pronounced gluc ose uptake showed a larger serum potassium decline and lowered aldosterone concentrations during induced euglycemic hyperinsulinemia. Insulin-resistan t patients showed a less pronounced reduction in FFA during hyperinsulinemi a, The observations in the present study may indicate that alterations in a ldosterone and FFA metabolism might be linked to the insulin resistance met abolic syndrome. (C) 2001 Lippincott Williams & Wilkins.