Effect of atrial natriuretic factor infusion on basal and CRH-stimulated ACTH, cortisol and aldosterone levels in patients with Cushing's or Addison's disease

B. Ambrosi, C. Sala, D. Bochicchio, P. Colombo, G. Gazzano, C. Fardin, A. Morganti, G. Faglia

Research output: Contribution to journalArticle

Abstract

Objective. While it has been shown that atrial natriuretic factor (ANF) is able to inhibit CRH-stimulated ACTH secretion in vitro, in normal men conflicting results on its effect on ACTH/cortisol responses to insulin and CRH have been reported. Since no data are available concerning the possible influence of ANF on the hypothalamic-pituitary-adrenal axis in states of ACTH hypersecretion, the effect of ANF on pituitary-adrenal function in basal conditions and after CRH stimulation has been investigated in patients with Cushing's (n=4) and Addison's disease (n = 4). Design. On two different days all patients underwent the following procedures: (a) α-human ANF was infused, after a priming dose of 100 ng i.v., at a rate of 0.01 μg/kg/min over 5 hours. After 120 minutes of ANF infusion, oCRH (1 μg/kg) was i.v. injected as a bolus; (b) vehicle infusion was given over 5 hours and at 120 minutes oCRH was injected. Plasma ANF, ACTH, cortisol, aldosterone, renin activity and K+ were measured; heart rate and blood pressure were monitored. Results. In Cushing's disease plasma ANF rapidly increased within 30 minutes of the exogenous peptide infusion (from 27 ± 5 to 73 ± 14 pmol/1; mean ± SE), whereas in the vehicle study its concentration was unchanged. During the first 2 hours of both tests no significant modifications in ACTH levels were observed. After CRH the plasma ACTH peak was unchanged. Serum cortisol levels progressively declined during the first 2 hours of ANF infusion (from 778 ± 150 to 461 ± 48 nmol/l; P+ were only slightly affected on both occasions. Conclusions. (1) In patients with corticotrophin hypersecretion ANF does not influence basal and CRH-stimulated ACTH secretion; (2) in Cushing's disease ANF inhibits cortisol and aldosterone basal secretion; this effect is not mediated by ACTH and is over-ridden by CRH stimulation.

Original languageEnglish
Pages (from-to)589-594
Number of pages6
JournalClinical Endocrinology
Volume40
Issue number5
Publication statusPublished - 1994

ASJC Scopus subject areas

  • Endocrinology

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