Search Results

You are looking at 1 - 1 of 1 items for

  • Author: K. L. Henville x
  • Refine by access: All content x
Clear All Modify Search
K. L. Henville
Search for other papers by K. L. Henville in
Google Scholar
PubMed
Close
,
J. P. Hinson
Search for other papers by J. P. Hinson in
Google Scholar
PubMed
Close
,
G. P. Vinson
Search for other papers by G. P. Vinson in
Google Scholar
PubMed
Close
, and
S. M. Laird
Search for other papers by S. M. Laird in
Google Scholar
PubMed
Close

ABSTRACT

The responses of human adrenocortical cells to stimulation by ACTH(1–24), desacetyl-α-MSH, α-MSH and angiotensin II amide have been compared. Both desacetyl-α-MSH, thought to be the major form of the peptide in the human pituitary and in circulating plasma, and α-MSH caused a significant stimulation of aldosterone, corticosterone and cortisol secretion. Significant stimulation of the production of these steroids was obtained with desacetyl-α-MSH at a concentration of 1 nmol/l, while the response to α-MSH was considerably less sensitive, with a minimum effective concentration of 0·1 μmol/l. These values compared with minimum effective concentrations of 1 pmol/l for ACTH and 0·1 μmol/l for angiotensin II amide. Although cell types were not separated, it is possible to conclude that none of the peptides showed any specificity for the zona glomerulosa, and in each case the same minimum effective concentration of peptide was required for both aldosterone and cortisol secretion. Yields of steroid obtained under conditions of maximal stimulation by ACTH(1–24), α-MSH and desacetyl-α-MSH were at least three to five times the basal output of aldosterone, four to eight times that for corticosterone and more than seven to sixteen times that for cortisol. Angiotensin II amide was a relatively poor stimulant with maximal stimulation only 1·5 × basal. In these experiments the minimum effective concentration for desacetyl-α-MSH (1 nmol/l) was close to the circulating concentration of desacetyl-α-MSH (0·3 nmol/l) in man, and it is thus possible that this peptide may have a physiological role in the control of adrenocortical function.

Journal of Endocrinology (1989) 121, 579–583

Restricted access