Nitric oxide synthesis inhibition blocks reversal of two-kidney, one clip renovascular hypertension after unclipping.
Nitric oxide synthesis inhibition blocks reversal of two-kidney, one clip renovascular hypertension after unclipping.
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一氧化氮合成抑制可阻断松解后两肾一夹肾血管性高血压的逆转。
DOI：
10.1161/01.hyp.25.2.174
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发表时间：
1995
期刊：
影响因子：
--
通讯作者：
Sigmon,DH
中科院分区：
文献类型：
--
作者：
Beierwaltes,WH;Potter,DL;Carretero,OA;Sigmon,DH
众所周知，两肾一夹肾血管性高血压可以通过松夹迅速逆转。我们假设，快速的肾脏再灌注和随后的血压下降部分是由内皮衍生的松弛因子一氧化氮介导的。我们用10 mg/kg体重的ω-硝基-L-精氨酸甲酯来检测NO合成抑制是否能阻断去夹闭引起的降压反应。在左肾动脉上放置银夹，造成大鼠高血压。4周后麻醉，不治疗(对照组)或一氧化氮合成阻断。10分钟后，取出夹子，监测血压超过60分钟。对照组初始血压为157±8 mm Hg，心率为310±21次/min。解除夹闭后，血压在45分钟内降至125±6毫米汞柱(P<；0.005)。心率不变(312±9次/分钟)。相反，一氧化氮合成抑制使血压从149±6毫米汞柱增加到174±9毫米汞柱(P<；.001)。去夹夹不改变血压，60分钟后血压为167±8毫米汞柱(与对照组相比P<；0.005)，心率保持不变(282±13次/分钟对276±16次/分钟)。我们用放射性微球测定了流向被剪断肾脏的血流量。未经治疗的高血压大鼠肾血流量增加10倍(P<；.001)，同时血压降低。在一氧化氮合成受到抑制的大鼠中，去夹闭导致肾脏血流量增加，仅为未治疗大鼠的三分之一，而血压没有变化。我们的结果表明，一氧化氮合成抑制消除了去夹夹引起的肾血管性高血压的急性逆转。提示内皮源性一氧化氮可能是两肾一夹肾血管性高血压逆转的重要组成部分，其机制可能是促进肾再灌流或介导肾再灌流后的全身反应。
It is well established that two-kidney, one clip renovascular hypertension can be rapidly reversed by unclipping. We hypothesized that rapid renal reperfusion and the subsequent fall in blood pressure are mediated in part by nitric oxide, the endothelium-derived relaxing factor. We tested whether the hypotensive response to unclipping could be blocked by nitric oxide synthesis inhibition using a bolus of 10 mg/kg body wtNω-nitro-l-arginine methyl ester. Rats were made hypertensive by placing a silver clip on the left renal artery. After 4 weeks, they were anesthetized and either not treated (controls) or had nitric oxide synthesis blockade. After 10 minutes, the clip was removed and blood pressure monitored over 60 minutes. Initial pressure in controls was 157±8 mm Hg, and heart rate was 310±21 beats per minute. Unclipping resulted in pressure falling to 125±6 mm Hg within 45 minutes (P<.005). Heart rate was unchanged (312±9 beats per minute). In contrast, nitric oxide synthesis inhibition increased blood pressure from 149±6 to 174±9 mm Hg (P<.001). Unclipping did not change blood pressure, which was 167±8 mm Hg after 60 minutes (P<.005 versus controls), and heart rate remained unchanged (282±13 versus 276±16 beats per minute). We determined the blood flow to the clipped kidneys using radioactive microspheres. Unclipping untreated hypertensive rats resulted in a 10-fold increase in renal blood flow (P<.001), concomitant with a decrease in blood pressure. In rats with nitric oxide synthesis inhibition, unclipping resulted in an increase in renal blood flow that was only a third of that seen in untreated rats, with no change in blood pressure. Our results show that nitric oxide synthesis inhibition eliminates the acute reversal of renovascular hypertension caused by unclipping. This suggests that endothelium-derived nitric oxide may be an important component in the reversal of two-kidney, one clip renovascular hypertension, either by facilitating renal reperfusion or by mediating the systemic response secondary to renal reperfusion.
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DOI：
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