[Studies on hypoaldosteronism associated with diabetes mellitus: response of plasma steroids to angiotensin II or ACTH administration].
This study was designed to clarify the cause of hyporeninemic hypoaldosteronism (HH) associated with diabetes mellitus. Fourty diabetic patients (DP) were divided into 3 groups; 12 patients without neuropathy or nephropathy, 13 with neuropathy and without nephropathy, and 15 with neuropathy and nephropathy; in the third group 3 HH patients were included. Fourteen normal subjects served as controls. In all DP and the normal subjects, plasma concentration of aldosterone (PAld), 18-hydroxycorticosterone (P18-OH-B), corticosterone (PB), 11-deoxycorticosterone (PDOC) and cortisol (PF) were measured before and after intravenous administration of angiotensin II (AII, 10 ng/kg/min, for 30 min) or ACTH (1-24 ACTH, 0.25 mg). In 27 DP, plasma renin activity (PRA) increased from 0.8 +/- 0.6 SD to 2.4 +/- 2.2 ng/ml/h (normal: 1.2 +/- 0.7 to 3.2 +/- 1.7 ng/ml/h) 2 hours after intravenous administration of furosemide (1 mg/kg) and assumption of the upright posture. No significant difference in PRA was found between DP and controls, whereas the response to these stimuli decreased significantly in 9 DP with neuropathy and nephropathy (from 0.4 +/- 0.2 to 0.7 +/- 0.4 ng/ml/h). The major results were as follows: 1) The mean of PAld (5.9 +/- 2.4 ng/100 ml) in DP was significantly lower than that in controls (7.7 +/- 2.2 ng/100 ml). There was no significant difference of PAld between DP without complications and controls. PAld in DP with neuropathy alone (5.0 +/- 1.5 ng/100 ml, p less than 0.05) and that in DP with neuropathy and nephropathy (4.7 +/- 2.4 ng/100 ml, p less than 0.05) were lower than that in controls. The mean of P18-OH-B (12.3 +/- 4.3 ng/100 ml) in DP was similar to that (14.2 +/- 3.2 ng/100 ml) in controls. P18-OH-B in DP without complications and that in DP with neuropathy alone were similar to that in controls. However, P18-OH-B (8.8 +/- 3.2 ng/100 ml) in DP with neuropathy and nephropathy was significantly lower than that in controls (p less than 0.001). No difference in PB, PDOC or PF was observed between DP and controls. 2) PAld increased from 6.0 +/- 2.5 ng/100 ml in DP (p less than 0.001) and from 7.6 +/- 2.2 to 15.7 +/- 5.3 ng/100 ml in controls (p less than 0.001) 30 min after A II infusion.(ABSTRACT TRUNCATED AT 400 WORDS)
D015069:18-Hydroxycorticosterone / Q000097:blood; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology*; D000328:Adult; D000368:Aged; D000450:Aldosterone / Q000097:blood*; D000804:Angiotensin II / Q000494:pharmacology*; D003345:Corticosterone / Q000097:blood*; D003900:Desoxycorticosterone / Q000097:blood; D003924:Diabetes Mellitus, Type 2 / Q000097:blood*; D003928:Diabetic Nephropathies / Q000097:blood; D003929:Diabetic Neuropathies / Q000097:blood; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood*; D008297:Male; D008875:Middle Aged; D012084:Renin-Angiotensin System / Q000187:drug effects
D000804:Angiotensin II; D003900:Desoxycorticosterone; D000450:Aldosterone; D015069:18-Hydroxycorticosterone; D000324:Adrenocorticotropic Hormone; D003345:Corticosterone; D006854:Hydrocortisone