Short-term ANG II produces renal vasoconstriction independent of TP receptor activation and TxA2/isoprostane production.
Short-term ANG II produces renal vasoconstriction independent of TP receptor activation and TxA2/isoprostane production.
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短期 ANG II 产生独立于 TP 受体激活和 TxA2/异前列烷产生的肾血管收缩。
DOI：
10.1152/ajprenal.00510.2006
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发表时间：
2007
期刊：
影响因子：
--
通讯作者：
Arendshorst,WilliamJ
中科院分区：
文献类型：
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作者：
Vågnes,ØyvindB;Iversen,BjarneM;Arendshorst,WilliamJ
血管收缩系统和血管扩张系统的相对作用在健康中是平衡的。这种平衡在疾病中被重置，通常有利于血管收缩剂的主导作用，这可能是由于收缩剂系统之间的积极相互作用。例如，在高血压中，慢性高水平的血管紧张素II（ANG II）刺激血栓烷（TxA 2/PGH 2）和/或异前列烷的产生，其激活血管系统中的收缩性血栓烷前列腺素（TP）受体。本研究评价了急性肾动脉给予中等浓度的ANG II对尿中TxB 2和异前列腺素排泄的影响，以及可能的肾TP受体激活可能放大ANG II诱导的肾血管收缩。TP受体被SQ 29548和ANG Ⅱ阻断。结果与持续ANG II输注（40 ng·min-1·kg体重-1）超过90 min的时间对照组进行比较。30-60 min期间TP受体拮抗剂对ANG II产生的肾血流量（RBF）减少无影响（15.8 ± 2.8 vs. 13.2 ± 4.9%）（P> 0.6）。同样，在有或无TP受体拮抗剂的情况下，ANG II诱导的肾血管收缩在60-90分钟之间没有差异（RBF −8.6 ± 4.0 vs. −9.6 ± 4.5%）（P> 0.8）。全身动脉压始终稳定，因此RBF变化反映了肾血管阻力的局部变化。ANG Ⅱ使尿中TxB 2和异前列腺素的排泄量增加近一倍。目前的数据表明，短期肾内输注血管紧张素II迅速增加肾生产的TxA 2，但血管紧张素II诱导的肾血管收缩是独立的TP受体激活在最初的90分钟的局部挑战与血管紧张素II。
The relative contributions of vasoconstrictor and of dilator systems are balanced in health. The balance is reset in disease, often favoring a predominant role of vasoconstrictors, perhaps due to positive interactions between constrictor systems. For example, in hypertension, chronic high levels of angiotensin II (ANG II) stimulate the production of thromboxane (TxA2/PGH2) and/or isoprostane that activate constrictor thromboxane prostanoid (TP) receptors in the vasculature. The present study evaluated a modest concentration of ANG II administered acutely into the renal artery on urinary excretion of TxB2and isoprostane and possible renal TP receptor activation that might amplify ANG II-induced renal vasoconstriction. TP receptors were blocked with SQ29548 coinfused with ANG II. Results were compared with a time control group of continuous ANG II infusion (40 ng·min−1·kg body wt−1) over 90 min. TP receptor antagonism during 30–60 min had no effect on the reduction in renal blood flow (RBF) produced by ANG II (15.8 ± 2.8 vs. 13.2 ± 4.9%) (P> 0.6). Likewise, there was no difference between groups during ANG II-induced renal vasoconstriction between 60–90 min in presence or absence of TP receptor antagonist (RBF −8.6 ± 4.0 vs. −9.6 ± 4.5%) (P> 0.8). Systemic arterial pressure was stable throughout, so RBF changes reflected localized changes in renal vascular resistance. Urinary excretion of TxB2and isoprostane were nearly doubled by ANG II. The present data indicate that short-term intrarenal infusion of ANG II rapidly increases renal production of TxA2but that the ANG II-induced renal vasoconstriction is independent of TP receptor activation during the initial 90 min of local challenge with ANG II.