Dopamine inhibits corticosteroid secretion from frog adrenal gland, in vitro.
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.
Morra
M
M
Laboratoire d'Endocrinologie Moléculaire, CNRS-URA 650, Faculté des Sciences, Université de Rouen, Mont-Saint-Aignan, France.
Leboulenger
F
F
Vaudry
H
H
D000305:Adrenal Cortex Hormones / Q000378:metabolism*; D000311:Adrenal Glands / Q000187:drug effects / Q000378:metabolism*; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology; D000450:Aldosterone / Q000378:metabolism; D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D001058:Apomorphine / Q000494:pharmacology; D003345:Corticosterone / Q000378:metabolism; D004298:Dopamine / Q000008:administration & dosage / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D004837:Epinephrine / Q000494:pharmacology; D066298:In Vitro Techniques; D007700:Kinetics; D008297:Male; D009638:Norepinephrine / Q000494:pharmacology; D011895:Rana ridibunda; D012701:Serotonin / Q000494:pharmacology
D000305:Adrenal Cortex Hormones; D000804:Angiotensin II; D012701:Serotonin; D000450:Aldosterone; D000324:Adrenocorticotropic Hormone; D001058:Apomorphine; D004298:Dopamine; D003345:Corticosterone; D009638:Norepinephrine; D004837:Epinephrine