|
|
||||||||
The effect of dopamine (1 µg/kg per min) on corticosteroid response to ACTH (0·1, 1 and 10 ng/kg per min) was compared with that of a placebo in sodium-replete (150 mmol/day) and -deplete (10 mmol/day) normal man. Dopamine had no effect on aldosterone, cortisol or corticosterone responses in either dietary phase, but increased deoxycorticosterone (897·0 ± 126·4 (S.E.M.) vs 590·0 ±84·3 pmol/l, normal Na+; 1264·2 ±84·3 vs 764·5 ±84·3 pmol/l, low Na+) and deoxycortisol (6·033 ± 0·583 vs 5·048±0·680 nmol/l, normal Na+; 5·112 ± 0·600 vs 4·130± 0·367 nmol/l, low Na+) levels during ACTH administration (all P <0·01). Deoxycorticosterone and corticosterone responses to ACTH were greater during sodium depletion than repletion (both P <0·01).
Dopamine therefore increased 11-deoxycorticosteroid concentrations during ACTH-stimulated steroidogenesis. This may reflect action of dopamine to increase extra-adrenal formation of 11-deoxycorticosteroids.
J. Endocr. (1986) 109, 339–344
This article has been cited by other articles:
![]() |
K. J. Biller, R. J. Unwin, and D. G. Shirley Distal tubular electrolyte transport during inhibition of renal 11{beta}-hydroxysteroid dehydrogenase Am J Physiol Renal Physiol, January 1, 2001; 280(1): F172 - F179. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | CONTACT US | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |