Interplay of various factors in glucose-induced hyperkalemia during captopril treatment.
The effect of angiotensin converting enzyme inhibition by captopril (CAP) on serum potassium (SK) changes was studied during a three-hour glucose tolerance test (GTT) in recumbent and upright positions in 16 patients with drug-resistant hypertension. An elevation of SK in the upright posture occurred in the course of GTT during CAP treatment in 50% of the patients (Group I) even without consistent changes in baseline SK. In Group II a qualitatively normal glucose-induced hypokalemic response was obtained. Aldosterone was suppressed by CAP, predominantly in the upright position in Group I due to the significant interaction between the drug and posture. Significant inverse correlations were found in Group I between glucose-induced serum potassium changes and basal glomerular filtration rate. A similar correlation was found also with serum insulin in the whole patient material. It was concluded that the interplay of various factors, CAP, upright posture and impaired renal functions resulting in suppression of aldosterone and insulin played a role in the paradoxical glucose-induced serum potassium elevation.
D000328:Adult; D000450:Aldosterone / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure / Q000187:drug effects; D002216:Captopril / Q000009:adverse effects* / Q000627:therapeutic use; D005919:Glomerular Filtration Rate; D005947:Glucose / Q000494:pharmacology*; D005951:Glucose Tolerance Test; D006801:Humans; D006947:Hyperkalemia / Q000139:chemically induced*; D006973:Hypertension / Q000188:drug therapy; D007328:Insulin / Q000097:blood; D007677:Kidney Function Tests; D008875:Middle Aged; D011188:Potassium / Q000097:blood; D012083:Renin / Q000097:blood
D001786:Blood Glucose; D007328:Insulin; D000450:Aldosterone; D002216:Captopril; D012083:Renin; D005947:Glucose; D011188:Potassium