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Role of COX-1 and -2 in prostanoid generation and modulation of angiotensin II responses.

机译:COX-1和-2在前列腺素生成和血管紧张素II反应调节中的作用。

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摘要

The role of cyclooxygenase (COX)-1 and -2 in prostanoid formation and modulation of pressor responses to ANG II was investigated in the pulmonary and systemic vascular beds in the rat. In the present study, selective COX-1 and -2 inhibitors attenuated increases in pulmonary arterial pressure and decreases in systemic arterial pressure in response to arachidonic acid but did not alter responses to PGE1 or U-46619. The selective COX-1 and -2 inhibitors did not modify systemic pressor responses to injections or infusions of ANG II or pulmonary pressor responses to injections of the peptide. COX-2 inhibitors did not alter, whereas a COX-1 inhibitor depressed, arachidonic acid-induced platelet aggregation. These data provide evidence in support of the hypothesis that prostanoid synthesis occurs by way of the COX-1 and -2 pathways in the pulmonary and systemic vascular beds but that pressor responses to ANG II are not mediated or modulated by these pathways in the rat.
机译:在大鼠的肺和全身血管床中研究了环氧合酶(COX)-1和-2在前列腺素形成和对ANG II的升压反应调节中的作用。在本研究中,选择性COX-1和-2抑制剂对花生四烯酸的响应减弱了肺动脉压的升高,而在全身动脉压方面则有所降低,但并未改变对PGE1或U-46619的响应。选择性COX-1和-2抑制剂不会改变对ANG II注射或输注的全身升压反应或对肽注射的肺升压反应。 COX-2抑制剂没有改变,而COX-1抑制剂抑制了花生四烯酸诱导的血小板凝集。这些数据提供了支持这样的假说的证据:前列腺素合成是通过肺和全身血管床中的COX-1和-2途径发生的,但是大鼠中对这些ANG II的升压反应没有被这些途径介导或调节。

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