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Prostaglandin F2α evokes vasoconstrictor and vasodepressor activities that are both independent of the F prostanoid receptor.
Zeng, Ruhui; Liu, Bin; Guo, Tingting; Guo, Jinwei; Yu, Gang; Xu, Yineng; Lin, Rui; Tan, Xiangzhai; Xie, Kaiqi; Zhou, Yingbi.
Afiliación
  • Zeng R; Department of Gynaecology and Obstetrics, First Affiliated Hospital, Shantou University Medical College, Shantou, China.
  • Liu B; Cardiovascular Research Center, Shantou University Medical College, Shantou, China.
  • Guo T; Cardiovascular Research Center, Shantou University Medical College, Shantou, China.
  • Guo J; Guangdong Provincial Key Laboratory of Infectious Diseases and Molecular Immunopathology, Shantou University Medical College, Shantou, China.
  • Yu G; Cardiovascular Research Center, Shantou University Medical College, Shantou, China.
  • Xu Y; Cardiovascular Research Center, Shantou University Medical College, Shantou, China.
  • Lin R; Guangdong Provincial Key Laboratory of Infectious Diseases and Molecular Immunopathology, Shantou University Medical College, Shantou, China.
  • Tan X; Cardiovascular Research Center, Shantou University Medical College, Shantou, China.
  • Xie K; Cardiovascular Research Center, Shantou University Medical College, Shantou, China.
  • Zhou Y; Cardiovascular Research Center, Shantou University Medical College, Shantou, China.
FASEB J ; 36(5): e22293, 2022 05.
Article en En | MEDLINE | ID: mdl-35349198
The F prostanoid receptor (FP), which accounts for the therapeutic effect of PGF2α in uterine atony that leads to postpartum hemorrhage and maternal morbidity, could possibly mediate vasoconstrictor effect in small or resistance arteries to elevate blood pressure that limits the clinical use of the agent in patients with cardiovascular disorders. This study aimed to test the above hypothesis with genetically altered mice. Ex vivo and in vivo experiments were performed on control wild-type (WT) mice and mice with deficiencies in FP (FP-/- ) or thromboxane (Tx)-prostanoid receptor (the original receptor of TxA2 ; TP-/- ), and/or those with an additional deficiency in E prostanoid receptor-3 (one of the vasoconstrictor receptors of PGE2 ; EP3-/- ). Here, we show that PGF2α indeed evoked vasoconstrictor responses in the above-mentioned tissues of WT mice, which were however unaltered by FP-/- . Interestingly, such contractile responses were reversed into dilations by TP-/- /EP3-/- . A similar pattern of results was observed with the pressor effect of PGF2α under in vivo conditions. However, TP-/- alone (which could largely remove the contractile responses) did not result in relaxation to PGF2α . Also, either the ex vivo vasodilator effect or the in vivo depressor response of PGF2α obtained after the removal of TP and EP3-mediated actions was unaltered by FP-/- . Therefore, both the ex vivo vasoconstrictor action in small or resistance arteries and the systemic pressor effect of PGF2α can reflect vasoconstrictor activities derived from the non-FP receptors TP and EP3 outweighing a concurrently activated dilator effect, which is again independent of FP.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Vasoconstrictores / Receptores de Prostaglandina Límite: Animals Idioma: En Revista: FASEB J Asunto de la revista: BIOLOGIA / FISIOLOGIA Año: 2022 Tipo del documento: Article País de afiliación: China Pais de publicación: Estados Unidos
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Vasoconstrictores / Receptores de Prostaglandina Límite: Animals Idioma: En Revista: FASEB J Asunto de la revista: BIOLOGIA / FISIOLOGIA Año: 2022 Tipo del documento: Article País de afiliación: China Pais de publicación: Estados Unidos