Angiotensin II constriction of rat vasa recta is partially thromboxane dependent.

Angiotensin II constriction of rat vasa recta is partially thromboxane dependent.
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血管紧张素II对大鼠直肠血管的收缩作用部分依赖于血栓素。

DOI:
10.1161/01.hyp.0000033467.04939.dd
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发表时间:
2002
期刊:
Hypertension (Dallas, Tex. : 1979)
影响因子:
--
通讯作者:
Pallone,ThomasL
Pallone,ThomasL
中科院分区:
--
文献类型:
--
作者:
Silldorff,ErikP;Hilbun,LaylaR;Pallone,ThomasL

文献摘要

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我们检验了血栓素的产生介导血管紧张素(Ang) II对离体外髓直降血管(OMDVR)的血管收缩的假设。脂氧合酶和环氧合酶(COX)抑制剂二十碳四酸(1 μmol/L)和COX抑制剂吲哚美辛(1 μmol/L)部分逆转Ang II (1 nmol/L)对体外灌注OMDVR的收缩。为了确定血栓素是否是Ang II诱导的血管收缩的介质,将血栓素合成酶抑制剂U63577A (1 μmol/L)和血栓素受体拮抗剂SQ-29548或bms - 180291(各1 μmol/L)引入到Ang II预收缩的血管液中。这些药物明显抑制Ang II诱导的血管收缩。相比之下,SQ-29548和U63557A通过将细胞外KCl从5提高到100 mmol/L,对血管预收缩没有影响。血栓素受体激动剂U46619 (1 μmol/L)能抑制OMDVR,而拮抗剂BMS-180,291能阻断这一作用。在不同的方案中,微灌注的OMDVR用U63577A或SQ-29548预处理,然后暴露于腔内Ang II以诱导血管收缩。两种药物均抑制血管收缩,无论是通过浴液还是灌注液。我们得出结论,Ang ii诱导的OMDVR的收缩部分是由花生四烯酸的代谢物介导的,包括血栓素。
We tested the hypothesis that thromboxane generation mediates vasoconstriction of isolated outer medullary descending vasa recta (OMDVR) by angiotensin (Ang) II. The lipoxygenase and cyclooxygenase (COX) inhibitor eicosatetraynoic acid (1 μmol/L) and the COX inhibitor indomethacin (1 μmol/L) partially reversed Ang II (1 nmol/L) constriction of in vitro perfused OMDVR. To determine whether thromboxane is a mediator of Ang II–induced vasoconstriction, a thromboxane synthase inhibitor, U63577A (1 μmol/L), and thromboxane receptor antagonists, SQ-29548 or BMS-180,291 (1 μmol/L, each), were introduced into the bath of vessels that had been preconstricted by Ang II (1 nmol/L). These agents significantly inhibited vasoconstriction induced by Ang II. In contrast, SQ-29548 and U63557A did not affect vessels preconstricted by raising extracellular KCl from 5 to 100 mmol/L. The thromboxane receptor agonist U46619 (1 μmol/L) constricted OMDVR, an effect that was blocked by the antagonist BMS-180,291. In separate protocols, microperfused OMDVR were pretreated with U63577A or SQ-29548, after which they were exposed to luminal Ang II to induce vasoconstriction. Both agents inhibited vasoconstriction whether preexposure to them was via the bath or the perfusate. We conclude that Ang II–induced constriction of OMDVR is partly mediated by metabolites of arachidonic acid, including thromboxanes.