title: Lack of enhanced responsiveness of plasma 18-hydroxycorticosterone and aldosterone to adrenocorticotropin as well as to angiotensin-II during moderate sodium depletion in type II diabetic subjects with normoreninemia.
abstract: Responses of plasma aldosterone (PA) and its precursor steroids to alpha ACTH-(1-24) (85.2 nmol, iv) injection and graded angiotensin-II (AII) infusions (3.90 and 7.80 pmol/kg.min for 30 min at each dose) on both 170 and 100 mmol sodium intakes were assessed in 25 type II diabetic subjects with normoreninemia and 11 age-matched normal subjects. The diabetic subjects and the normal subjects did not differ in mean blood pressure, serum electrolytes, and creatinine clearance, except for an increase in fasting plasma glucose (P less than 0.001) in the diabetic subjects. A 100-mmol sodium intake for 4 days produced an increase in basal plasma renin activity (P less than 0.01), plasma 18-hydroxycorticosterone (18-OHB; P less than 0.05), and PA (P less than 0.05), and a decrease in urinary sodium excretion (P less than 0.001) in the two groups. These parameters were similar in the two groups. ACTH injection produced significant increases in plasma cortisol, plasma corticosterone, plasma 18-OHB, and PA (P less than 0.005 or P less than 0.001), and graded AII infusions produced significant increases in plasma 18-OHB and PA (P less than 0.05 or P less than 0.01) during both 170- and 100-mmol sodium intakes in the two groups. In the diabetic subjects, however, the responses of plasma 18-OHB and PA to both ACTH injection and graded AII infusions on a 100-mmol, but not on a 170-mmol, sodium intake were subnormal (P less than 0.05 or P less than 0.01) and were similar to those on a 170-mmol sodium intake. These results indicate a lack of enhanced responsiveness of plasma 18-OHB and PA to both ACTH and AII during moderate sodium restriction in nonazotemic type II diabetic subjects with normoreninemia. It appears that these subjects have selective unresponsiveness of adrenal zona glomerulosa to sodium depletion per se, but not to ACTH or AII.
authors.affiliation: Department of Internal Medicine, Kanazawa Medical University, Ishikawa, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Kigoshi
authors.forename: R
authors.initials: R
authors.lastname: Iwasaki
authors.forename: M
authors.initials: M
authors.lastname: Kaneko
authors.forename: S
authors.initials: S
authors.lastname: Nakano
authors.forename: S
authors.initials: S
authors.lastname: Azukizawa
authors.forename: K
authors.initials: K
authors.lastname: Uchida
authors.forename: S
authors.initials: S
authors.lastname: Morimoto
mesh_terms: D015069:18-Hydroxycorticosterone / Q000097:blood*; D000305:Adrenal Cortex Hormones / Q000097:blood; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology*; D000328:Adult; D000368:Aged; D000450:Aldosterone / Q000097:blood*; D000804:Angiotensin II / Q000494:pharmacology*; D001794:Blood Pressure / Q000187:drug effects; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000378:metabolism / Q000503:physiopathology; D004702:Endocrine Glands / Q000503:physiopathology; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D012016:Reference Values; D012083:Renin / Q000097:blood; D012964:Sodium / Q000172:deficiency* / Q000494:pharmacology
chemical_list: D000305:Adrenal Cortex Hormones; D000804:Angiotensin II; D000450:Aldosterone; D015069:18-Hydroxycorticosterone; D000324:Adrenocorticotropic Hormone; D012964:Sodium; D012083:Renin