Search Results

You are looking at 1 - 2 of 2 items for

  • Author: S. Al-Damluji x
  • Refine by Access: All content x
Clear All Modify Search
Restricted access

S. Al-Damluji

Department of Endocrinology, St Bartholomew's Hospital, London EC1A 7BE RECEIVED 29 January 1988


During the last 50 years, the role of adrenergic mechanisms in the control of secretion of corticotrophin (ACTH) has aroused much interest but little consensus. In view of recent advances in our understanding of the anatomy and physiology of catecholamine systems and improvements in pharmacological and experimental techniques, it has become possible to offer explanations or alternative interpretations for some of the apparently contradictory data. A clearer picture is emerging, although hazy areas remain.

Anatomical relationships

A close anatomical relationship exists between the central adrenergic and noradrenergic systems and the major hypothalamic peptides that are involved in the regulation of ACTH secretion, corticotrophin-releasing factor (CRF-41) and vasopressin. The cell bodies of the catecholaminergic neurones that innervate the parvocellular neurones of the paraventricular nucleus are found in the brain stem (Ungerstedt, 1971; Sawchenko

Restricted access

S. Al-Damluji, D. Cunnah, A. Grossman, L. Perry, G. Ross, D. Coy, L. H. Rees, and G. M. Besser


Six normal male subjects were given, in single blind random order on six separate occasions, i.v. bolus doses of synthetic ovine corticotrophin-releasing factor-41 (oCRF-41; 25 and 50 μg) with and without adrenaline (3 μg/min) i.v. for 150 min, the adrenaline infusions alone and saline placebo. The adrenaline infusions resulted in plasma adrenaline concentrations of 4·33 ± 0·82 (s.e.m.) nmol/l and were associated with an increase in blood glucose, heart rate and systolic blood pressure and a reduction of diastolic blood pressure. Despite these evident biological effects at several sites, there was no stimulation of plasma ACTH or cortisol by adrenaline in comparison with the effect of saline, and no enhancement of the stimulatory effect of either dose of oCRF-41 on ACTH or cortisol secretion. The ACTH response to 50 μg oCRF-41 was greater than that to 25 μg, indicating that the 25 μg dose of oCRF-41 was sub-maximal and capable of further enhancement. As the plasma adrenaline concentrations during the adrenaline infusions reached the upper limit of the physiological range of plasma adrenaline in man, yet failed to enhance the ACTH or cortisol responses to a sub-maximal dose of oCRF-41, we conclude that circulating adrenaline neither exerts a direct stimulatory effect on pituitary corticotrophs nor enhances the effect of CRF under physiological circumstances. The adrenaline infusions attenuated the ACTH and cortisol responses to oCRF-41 and were associated with a transient reduction of basal concentrations of both hormones.

J. Endocr. (1987) 112, 145–150