Role of adrenergic receptor subtypes in the control of human placental blood vessels.
The use of beta2-Adrenergic Receptor (AR) agonists and the potential use of alpha1-AR blockers as tocolytics raise the question of how they influence placental circulation. The receptor profile was characterized via the amounts of the mRNA of alpha1-AR subtypes and beta2-ARs. The mRNAs were detected by reverse transcription-polymerase chain reaction. Electric field stimulation (EFS) was applied to test the pharmacological reactivity of the placental vessels. Expressions of beta2- and all subtypes of alpha1-AR mRNA were demonstrated in human placental vessels, and were significantly higher in the arteries. A significant difference was not found between the veins and the arteries as concerns the amount of alpha1D-AR mRNA. There was a preponderance of alpha1A- and alpha1B-AR mRNA as compared to alpha1D-AR mRNA both in the arteries and in the veins. beta2-AR agonists and alpha1-AR antagonists antagonized the EFS-induced contractions of the placental arteries in a dose-dependent manner. These effects were significantly less marked on veins at all applied doses. Urapidil antagonized the EFS-induced contractions of both the placental arterial and vein rings in a dose-dependent manner. The beta2-, alpha1A-, and alpha1B-AR are the important subtypes involved in the regulation of the contractility of the human term placental vessels. The possible increase in placental blood flow mediated by these ARs can even be beneficial during pregnancy. Accordingly, the use of beta2-AR agonists and the potential use of alpha1-blockers as tocolytics seem safe on the basis of in vitro examinations as concerns the placental circulation.
Resch
Béla Endre
BE
Department of Pharmacodynamics and Biopharmacy, University of Szeged, Szeged, Hungary.
Ducza
Eszter
E
Gáspár
Róbert
R
Falkay
George
G
D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D001158:Arteries / Q000502:physiology; D004558:Electric Stimulation; D005260:Female; D015870:Gene Expression; D006801:Humans; D066298:In Vitro Techniques; D010920:Placenta / Q000098:blood supply* / Q000378:metabolism*; D011247:Pregnancy; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D018340:Receptors, Adrenergic, alpha-1 / Q000235:genetics / Q000502:physiology*; D018343:Receptors, Adrenergic, beta-2 / Q000235:genetics / Q000502:physiology*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014158:Transcription, Genetic; D014661:Vasoconstriction; D014680:Veins / Q000502:physiology
D000317:Adrenergic alpha-Antagonists; D012333:RNA, Messenger; D018340:Receptors, Adrenergic, alpha-1; D018343:Receptors, Adrenergic, beta-2