Mechanisms of signal transduction for adenosine and ATP in pulmonary vascular bed.
Mechanisms of signal transduction for adenosine and ATP in pulmonary vascular bed.
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肺血管床中腺苷和ATP的信号转导机制。
DOI：
10.1152/ajpheart.1992.262.3.h926
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发表时间：
1992
期刊：
影响因子：
--
通讯作者：
Hyman,A
中科院分区：
文献类型：
--
作者：
Lippton,HL;Hao,Q;Hauth,T;Hyman,A
本研究的目的是探讨百日咳毒素（PTX）敏感的鸟嘌呤核苷酸（G）蛋白在肺血管反应腺苷和ATP在完整的猫在控制肺血流和左心房压力的条件下的贡献。腺苷、ATP和β-tau-ATP以剂量依赖性方式增加肺叶动脉压。腺苷对肺血管的收缩作用可被特异性嘌呤能受体（P1）抑制剂BW 1433 U、PTX预处理、吲哚美辛和血栓素A2（TxA 2）受体拮抗剂ONO 3708所阻断。这些数据表明，肺血管收缩反应腺苷依赖于激活P1嘌呤受体耦合PTX敏感的G蛋白和随后的代谢释放的花生四烯酸形成TxA 2。由于研究的每种阻断剂在不改变肺血管收缩剂对β-tau-ATP的反应的情况下，对ATP的肺血管收缩反应产生类似的降低，因此目前的数据表明，ATP部分通过水解为腺苷来收缩肺血管床。此外，本研究表明，A1嘌呤受体与PTX敏感的G蛋白以及P2 x嘌呤受体是独立的PTX不敏感的G蛋白介导的肺血管收缩反应ATP在体内。
The purpose of the present study was to investigate the contribution of pertussis toxin (PTX)-sensitive guanine nucleotide (G) proteins in the pulmonary vascular response to adenosine and ATP in the intact cat under conditions of controlled pulmonary blood flow and left atrial pressure. Adenosine, ATP, and beta-tau-ATP increased lobar arterial pressure in a dose-dependent manner. The pulmonary vasoconstrictor response to adenosine was abolished by BW 1433U, a specific purinergic receptor (P1) inhibitor, PTX pretreatment, indomethacin, and ONO 3708, a thromboxane A2 (TxA2) receptor antagonist. These data suggest that the pulmonary vasoconstrictor response to adenosine depends on activation of P1 purinergic receptors coupled to PTX-sensitive G proteins and subsequent metabolism of liberated arachidonic acid to form TxA2. Because each blocking agent studied produced similar reductions in the pulmonary vasoconstrictor response to ATP without altering the pulmonary vasoconstrictor response to beta-tau-ATP, the present data suggest that ATP constricts the pulmonary vascular bed, in part, by hydrolysis to adenosine. Moreover, the present study suggests that both A1 purinoceptors that are linked to PTX-sensitive G proteins as well as P2x purinoceptors receptors that are independent of PTX-insensitive G proteins mediate the pulmonary vasoconstrictor response to ATP in vivo.