Endocrinology, Vol 127, 218-226, Copyright © 1990 by Endocrine Society

ARTICLES

Dopamine inhibits corticosteroid secretion from frog adrenal gland, in vitro

M Morra, F Leboulenger and H Vaudry
Laboratoire d'Endocrinologie Moleculaire, CNRS-URA 650, Faculte des Sciences, Universite de Rouen, Mont-Saint-Aignan, France.

The effect of dopamine on corticosteroid secretion from frog interrenal (adrenal) tissue was investigated in vitro using a perifusion system technique. Administration of graded concentrations of dopamine (5 X 10(- 8) M to 10(-3) M) to interrenal slices induced a dose-dependent inhibition of steroid secretion. The half-maximal effective dose of dopamine was 7 X 10(-6) M for corticosterone and 4 X 10(-6) M for aldosterone. Noradrenaline and adrenaline were also able to elicit a dose-related inhibition of steroid release, but these catecholamines were approximately 100 and 2000 times less potent than dopamine in our model. Administration of repeated pulses of dopamine (5 X 10(-5) M), at 150-min intervals, led to a reproducible inhibition of corticosteroid secretion without any desensitization phenomenon. Similarly, prolonged infusion of dopamine (5 X 10(-6) M) caused a sustained inhibition of steroidogenesis. The inhibitory action of dopamine was also observed using enzymatically dispersed adrenal cells, indicating that dopamine exerts a direct effect on adrenocortical cells. After the second pulse, dopamine also induced a transient stimulation of steroid secretion from acutely dispersed cells. Administration of short pulses of apomorphine (5 X 10(-5) M) induced a transient inhibition of corticosteroid secretion, and the kinetics of the response were very similar to that observed with dopamine. During prolonged administration of dopamine, the steroidogenic actions of ACTH (10(-9) M) and serotonin (5 X 10(-6) M) were not altered. In contrast, dopamine induced a marked inhibition of angiotensin II-evoked corticosteroid secretion. Taken together, these results show that the neurotransmitter dopamine exerts a direct inhibitory effect on steroid secretion from frog adrenocortical cells. Our results also indicate that dopamine and angiotensin II likely act through a common intracellular pathway. These data suggest that dopamine, released by chromaffin cells during neurogenic stress, may modulate the response of adrenocortical cells through a paracrine mode of communication.

This article has been cited by other articles:

				M. Ehrhart-Bornstein, J. P. Hinson, S. R. Bornstein, W. A. Scherbaum, and G. P. Vinson Intraadrenal Interactions in the Regulation of Adrenocortical Steroidogenesis Endocr. Rev., April 1, 1998; 19(2): 101 - 143. [Abstract] [Full Text]