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 Arthritis, Diabetes, Digestive and Kidney Diseases (NIADDK)
Type
Research Project (R01)
Project #
5R01AM006415-24
Application #
3150723
Study Section
Cardiovascular and Pulmonary Research B Study Section (CVB)
Project Start
1977-09-01
Project End
1987-08-31
Budget Start
1985-09-01
Budget End
1986-08-31
Support Year
24
Fiscal Year
1985
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

Biglieri, E G; Irony, I; Kater, C E (1989) Identification and implications of new types of mineralocorticoid hypertension. J Steroid Biochem 32:199-204
Kater, C E; Biglieri, E G; Brust, N et al. (1989) Stimulation and suppression of the mineralocorticoid hormones in normal subjects and adrenocortical disorders. Endocr Rev 10:149-64
Biglieri, E G; Irony, I; Kater, C E (1989) The regulation of the 17-deoxy steroids in man. Endocr Res 15:183-201
Pacifici, R; Perry 3rd, H M; Shieber, W et al. (1987) Adrenal responses to subtotal parathyroidectomy for primary hyperparathyroidism. Calcif Tissue Int 41:119-23
Irony, I; Biglieri, E G; Perloff, D et al. (1987) Pathophysiology of deoxycorticosterone-secreting adrenal tumors. J Clin Endocrinol Metab 65:836-40
Membreno, L; Irony, I; Dere, W et al. (1987) Adrenocortical function in acquired immunodeficiency syndrome. J Clin Endocrinol Metab 65:482-7
Lim Jr, R C; Nakayama, D K; Biglieri, E G et al. (1986) Primary aldosteronism: changing concepts in diagnosis and management. Am J Surg 152:116-21
Biglieri, E G; Kater, C E; Arteaga, E A (1986) Mineralocorticoid hypertension due to hyperaldosteronism and hyperdeoxycorticosteronism. J Hypertens Suppl 4:S61-5
Schambelan, M; Sebastian, A (1985) [Type IV renal tubular acidosis: pathogenetic role of aldosterone deficiency and hyperkalemia] Nephrologie 6:135-7
Arteaga, E; Klein, R; Biglieri, E G (1985) Use of the saline infusion test to diagnose the cause of primary aldosteronism. Am J Med 79:722-8

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