Glucose-induced hyperkalemia developing in the upright position in captopril-treated hypertensives

Paradoxical glucose-induced hyperkalemia (GIH) was elicited exclusively in the upright position during captopril treatment in four hypertensive patients (Group 3) without impaired glucose tolerance in three. Inhibited aldosterone production and inappropriate plasma aldosterone responses to increasing serum potassium may have been responsible for the captopril potentiated GIH. Similar GIH was found in four non-insulin dependent diabetic control patients with mineralocorticoid insufficiency (Group 1) but without captopril treatment, which could be prevented by desoxycorticosterone. Normal serum potassium responses to glucose, uninfluenced by desoxycorticosterone were shown in four untreated hypertensive control patients (Group 2).