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Endothelium-derived dopamine modulates EFS-induced contractions of human umbilical vessels
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  • José Britto-Júnior,
  • David Pinheiro,
  • Alberto Justo,
  • Guilherme Murari,
  • Rafael Campos,
  • Fernanda Mariano,
  • Valéria Souza,
  • André Schenka,
  • Fabiola Monica,
  • EDSON ANTUNES,
  • Gilberto de Nucci
José Britto-Júnior
UNICAMP
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David Pinheiro
State University of Campinas
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Alberto Justo
State University of Campinas
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Guilherme Murari
State University of Campinas
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Rafael Campos
State University of Ceara
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Fernanda Mariano
State University of Campinas
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Valéria Souza
State University of Campinas
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André Schenka
State University of Campinas
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Fabiola Monica
State University of Campinas
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EDSON ANTUNES
State University of Campinas
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Gilberto de Nucci
State University of Campinas
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Abstract

Background and purpose: Electrical field stimulation (EFS) induces contractions of both snake aorta and human umbilical cord vessels (HUCV) which were dependent on the presence of the endothelium. This study aimed to establish the nature of the mediator(s) responsible for EFS-induced contractions in HUCV. Experimental approach: Rings with or without endothelium from human umbilical artery (HUA) or vein (HUV) were mounted in organ bath chambers containing oxygenated, heated Krebs-Henseleit’s solution. Basal release of dopamine (DA), noradrenaline and adrenaline were measured by LC-MS-MS. Cumulative dose-response curves were performed with dopamine in the absence and in the presence of L-NAME or of dopamine antagonists. EFS studies were performed in the presence and absence L-NAME, the alpha-adrenergic blockers prazosin and idazoxan and the dopamine antagonists SCH-23390 and haloperidol. Tyrosine hydroxylase (TH) and dopa-decarboxylase (DDC) were studied by immunohistochemistry and fluorescence in-situ hybridizations. Key Results: Basal release of dopamine requires an intact endothelium in both HUA and HUV. TH and DDC are present only in the endothelium of both HUA and HUV as determined by immunohistochemistry. Dopamine induced contractions in HUA only in the presence of L-NAME. Dopamine-induced contractions in HUV were strongly potentiated by L-NAME. The EFS-induced contractions in both HUA and HUV were potentiated by L-NAME and inhibited by the D2-like receptor antagonist haloperidol. The α-adrenergic antagonists prazosin and idazoxan and the D1-like receptor antagonist SCH-23390 had no effect on the EFS-induced contractions of HUA and HUV. Conclusion and Implications: Endothelium-derived dopamine is a major modulator of HUCV reactivity in vitro.