SOME METABOLIC ASPECTS OF ESSENTIAL-HYPERTENSION AND ITS TREATMENT

We tested whether patients with essential hypertension (EH) have metab olic evidence of increased adrenergic activity, and if a relationship exists between carbohydrate metabolism and the blood pressure (BP) res ponse to angiotensin-converting enzyme (ACE) inhibition. Study 1 inclu ded 59 subjects who underwent resting ambulatory BP, heart rate, and r esting energy expenditure (REE) measurement (by indirect calorimetry). REE was directly related to lean body mass (LBM) (r = 0.56, p < 0.000 1) and to fasting plasma insulin levels (p < 0.03), after adjusting fo r LBM and age) but not to BP. The 38 subjects with EH had significantl y higher fasting plasma insulin levels (54 +/- 4 vs 42 +/- 4 pM; p < 0 .05) than the 21 normotensive subjects. When normalized by the LBM, th e hypertensive patients had significantly higher REE values than the n ormotensive subjects (89 +/- 2 vs 78 +/- 3 J min-1 . kg-1; p < 0.005). No differences in the other measured variables were found between the two groups. Thus, in this group of lean patients with stable EH, rela tive hyperinsulinemia is associated with a small increase in REE, the significance of which remains to be determined. In study 2, 20 patient s with EH received an oral glucose tolerance test and a euglycemic ins ulin clamp before and after 3 months of treatment with cilazapril. Glu cose-induced insulin response, but not insulin sensitivity, was improv ed by treatment in the whole group. Before therapy, the 12 responders (diastolic BP <95 mm Hg) had similar glucose tolerance and insulin sen sitivity to the eight nonresponders. Responders, however, had lower fr actional potassium excretion than nonresponders both during fasting (9 .6 +/- 1 vs 16.0 +/- 2.4%; p < 0.02) and during the glucose load (9.1 +/- 1.4 vs 13.1 +/- 1.1%; p < 0.04). In the responders, fasting potass ium levels at baseline were directly related to the decrease in BP (p < 0.01) and to the improvement of glucose-induced insulin response (p < 0.04) achieved after treatment. Thus, the therapeutic effect of ACE inhibition is in part related to fractional potassium excretion, which , in turn, affects glucose tolerance through the influence of potassiu m levels on glucose-induced insulin release.