Long-term captopril therapy with no effect on glucose metabolism in patients with essential hypertension.

The long-term antihypertensive response to captopril (25-50 mg/day) and 75g oral glucose tolerance (75g oGTT) following a 6-10 month period of captopril administration was evaluated in 20 patients with essential hypertension without persistent proteinuria. Eleven of these 20 patients exhibited impaired glucose tolerance (IGT), while the remaining nine patients had normal glucose tolerance (NGT). All patients tolerated long-term captopril therapy with no untoward effects. Six months' administration of captopril significantly decreased blood pressure in patients with NGT from 171 +/- 12/105 +/- 5 mm Hg (mean +/- SE) to 146 +/- 7/88 +/- 4 mm Hg. Also in patients with IGT, long-term captopril therapy decreased blood pressure from 165 +/- 3/97 +/- 2 to 143 +/- 5/86 +/- 2 mm Hg. No patient with NGT developed diabetes mellitus. Neither fasting nor post-glucose-load venous blood glucose deteriorated in any of the patients during the therapy. There were no significant changes in the insulinogenic index (delta IRI/delta BG at 30 minutes after glucose load) in both the patients with NGT and IGT. In patients with IGT, the concentration of glycosylated hemoglobin (Hb A1 and Hb A1c slightly but significantly decreased from 8.1 +/- 0.3 to 7.7 +/- 0.4% (P less than 0.05) and from 5.9 +/- 0.3 to 5.5 +/- 0.3% (P less than 0.01) after 6.2 +/- 1.4 months' captopril therapy. These results suggest that in addition to its antihypertensive effects, long-term captopril therapy does not compromise glucose metabolism in hypertensive patients.