Response of antidiuretic hormone to chlorpropamide.

Response of antidiuretic hormone to chlorpropamide Chlorpropamide has been used to treat diabetes insipidus since 1966,1 but its mode of action is still not entirely clear. There is good agreement that it augments the renal effects of endogenous antidiuretic hormone,2 but it might also cause pituitary release.3 To help clarify this we have measured serial plasma concentrations of antidiuretic hormone in a group of patients receiving long-term chlorpropamide. Eleven patients with maturity-onset diabetes (two women; age range 38-66 years, mean 56 years) requiring treatment with oral hypoglycaemics were studied. All were receiving conventional dietary advice. Blood was taken from an antecubital vein (after 30 minutes' sitting and overnight fast) before and four, eight, and 12 weeks after they started taking 250 mg chlorpropamide daily. Plasma concentrations of antidiuretic hormone were measured by radioimmunoassay (normal range 4-12 jtg/l). This method is reliable in assaying both normal and raised concentrations.4 Serum sodium and plasma glucose concentrations were measured by routine automated analysis. No change in chlorpropamide dosage was made during the study. All patients had normal renal function. Changes in measurements were assessed by Student's t test. Serum sodium concentration did not change throughout the study (figure), and no patient developed hyponatraemia. Blood glucose concentration had fallen significantly by four weeks (p<0001) but was unchanged thereafter. Plasma osmolality stayed within the normal range throughout the study. Plasma concentrations of antidiuretic hormone did not change significantly during the study.