Dopamine-stimulated adenylate cyclase in human term placenta.
The effect of dopamine on adenylate cyclase activity was investigated in slices of human term placentas. Dopamine elicited a dose-dependent stimulation of cAMP formation with a ED50 value of about 1 X 10(-6)M dopamine and an increase of 110% over the control with 1 X 10(-4)M dopamine. (-)-Epinephrine and (-)-norepinephrine also increased placental cAMP formation. Apomorphine displayed a slight but non-significant stimulatory effect while bromocriptine was not effective. SCH 23390, a selective antagonist of dopamine D1 receptors caused a dose-dependent decrease of the dopamine activation. In contrast, the dopamine increase of cAMP was unaffected by beta- and alpha-adrenergic blocking drugs and by the D2 selective antagonist, (-)-sulpiride. These data indicate that dopamine stimulates cAMP formation in human term placenta through a specific mechanism via D1 dopaminergic receptors positively coupled to adenylate cyclase.
D000262:Adenylyl Cyclases / Q000378:metabolism*; D002395:Catecholamines / Q000494:pharmacology; D004298:Dopamine / Q000502:physiology*; D018492:Dopamine Antagonists; D004789:Enzyme Activation / Q000187:drug effects; D005260:Female; D006801:Humans; D066298:In Vitro Techniques; D010920:Placenta / Q000201:enzymology*; D011247:Pregnancy; D011954:Receptors, Dopamine / Q000187:drug effects; D013565:Sympatholytics / Q000494:pharmacology
D002395:Catecholamines; D018492:Dopamine Antagonists; D011954:Receptors, Dopamine; D013565:Sympatholytics; D000262:Adenylyl Cyclases; D004298:Dopamine