Abstract

(DOC), corticosterone (B), and 18-hydroxydeoxycorticosterone (18-OHDOC) have a major role in regulating body electrolyte composition and blood pressure. The plasma measurement of 18-hydroxycorticosterone (18-OHB), the major penultimate precurosr of A, in addition to the earlier ones, DOC and B, is being used to further hyperplasia and hyperaldosteronism. 18-PHB levels are always high (greater than 100 ng/dl) and B and DOC elevations occur only in patients with adenoma. A decreasing plamsa potassium concentration reduces conversion of 18-OHB to A. The continued administration of ACTH in superphysiologic doses produces three patterns. DOC rises and remains elevated. B & 18-OHDOC show an initial rise followed after 24 hrs by a reduction to 28-60% of initial peak values. Both A and 18-OHB rise during first 24 hrs and then return to near control levels. ACTH impedes 11 beta and 18-hydroxylation as the mechanism for reduction of aldosterone and 11 beta and 18-hydroxylation as the mechanism for reduction of aldosterone and 11 beta and and 18 hydroxylations are likely to be the same enzyme. ACTH is likely to have inhibitory activity on aldosterone production at physiologic levels.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Type
Research Project (R01)
Project #
5R01DK006415-25
Application #
3224481
Study Section
Cardiovascular and Pulmonary Research B Study Section (CVB)
Project Start
1977-09-01
Project End
1987-08-31
Budget Start
1986-09-01
Budget End
1987-08-31
Support Year
25
Fiscal Year
1986
Total Cost
Indirect Cost

  Institution

Name
University of California San Francisco
Department
Type
Schools of Medicine
DUNS #
073133571
City
San Francisco
State
CA
Country
United States
Zip Code
94143

  Publications

Kater, C E; Biglieri, E G; Irony, I (1992) Low sodium intake enhances sensitivity of 11-deoxycortisol and deoxycorticosterone to ACTH in ACTH-suppressed normal subjects. J Steroid Biochem Mol Biol 42:617-23
Biglieri, E G; Kater, C E (1991) Steroid characteristics of mineralocorticoid adrenocortical hypertension. Clin Chem 37:1843-8
Farese Jr, R V; Biglieri, E G; Shackleton, C H et al. (1991) Licorice-induced hypermineralocorticoidism. N Engl J Med 325:1223-7
Biglieri, E G; Kater, C E (1991) 17 alpha-hydroxylation deficiency. Endocrinol Metab Clin North Am 20:257-68
Kater, C E; Irony, I; Biglieri, E G et al. (1990) Continuous adrenocorticotropin administration in hypopituitarism produces asynchronous increases of deoxycorticosterone and 11-deoxycortisol relative to other reduced zona fasciculata steroids. J Clin Endocrinol Metab 71:305-10
Irony, I; Kater, C E; Biglieri, E G et al. (1990) Correctable subsets of primary aldosteronism. Primary adrenal hyperplasia and renin responsive adenoma. Am J Hypertens 3:576-82
Biglieri, E G; Arteaga, E; Kater, C E (1987) Effect of ACTH on aldosterone and other mineralocorticoid hormones. Ann N Y Acad Sci 512:426-37
Schambelan, M; Sebastian, A; Katuna, B A et al. (1987) Adrenocortical hormone secretory response to chronic NH4Cl-induced metabolic acidosis. Am J Physiol 252:E454-60