Renal hemodynamic and excretory responses in anesthetized rats to FK409, a novel nitric oxide donor.

Renal hemodynamic and excretory responses in anesthetized rats to FK409, a novel nitric oxide donor.
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麻醉大鼠对 FK409(一种新型一氧化氮供体)的肾血流动力学和排泄反应。

DOI:
10.1016/s0014-2999(96)00945-4
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发表时间:
1997
影响因子:
5
通讯作者:
S. Morimoto
S. Morimoto
中科院分区:
医学2区
文献类型:
--
作者:
K. Urabe;Y. Matsumura;M. Nishiura;K. Maeda;S. Morimoto

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在麻醉大鼠上观察了(±)-(E)-4-乙基-2-[(E)-羟基亚氨基]-5-硝基-3-己烯酰胺(FK 409)对一氧化氮(NO)供体的肾血流动力学和排泄反应。以10 μ g/kg/min的剂量向正常大鼠肾动脉输注FK 409时,观察到中度肾脏血管扩张作用,平均动脉血压下降。与各对照值相比,尿流量、尿钠排泄量和钠排泄分数分别显著增加约85%、110%和75%。同时,尿中NO代谢产物(UNOxV)的排泄量随着FK409的给药而显著增加。在用NO合成酶抑制剂NG-硝基-L-精氨酸(NOARG)治疗的高血压大鼠中,FK409产生了有效的肾血管舒张作用,尽管该药物的扩张作用与正常大鼠相当。此外,肾小球滤过率显着升高的代理。排泄反应明显增加,即,尿流量、尿钠排泄和钠排泄分数的水平分别增加到每个对照值的约3倍、6倍和5倍。UNOxV的增加程度与正常大鼠相似。这些结果清楚地表明,FK 409通过NO形成引起肾血管舒张和利尿。肾血流动力学和排泄反应的代理是敏感的NO耗竭条件。在基础NO形成受损的情况下,FK 409和相关化合物可用于治疗肾病。
Renal hemodynamic and excretory responses to (±)-(E)-4-ethyl-2-[(E)-hydroxyimino]-5-nitro-3-hexenamide (FK409), a novel nitric oxide (NO) donor, were examined using anesthetized rats. When FK409 was infused into the renal artery of normal rats at 10 μg/kg per min, a moderate renal vasodilating effect was observed with a decrease in mean arterial blood pressure. Urine flow, urinary excretion of sodium and fractional excretion of sodium significantly increased by about 85%, 110% and 75%, respectively, compared with each control value. Simultaneously, urinary excretion of NO metabolites (UNOxV) was markedly increased with the administration of FK409. In hypertensive rats treated with NG-nitro-l-arginine (NOARG), the NO synthase inhibitor, FK409 produced a potent renal vasodilation, although the hypotensive effect of the agent was comparable to that seen in normal rats. In addition, glomerular filtration rate was significantly elevated by the agent. There were marked increases in the excretory responses, i.e., levels of urine flow, urinary excretion of sodium and fractional excretion of sodium were increased to about 3-, 6- and 5-fold of each control value, respectively. The extent of increment of UNOxV was similar to that seen in normal rats. These results clearly indicate that FK409 causes renal vasodilation and diuresis, via NO formation. Renal hemodynamic and excretory responses to the agent are sensitive in NO-depleted conditions. FK409 and related compounds may be useful for the treatment of renal diseases, in cases where the basal NO formation is impaired.
内皮源性舒张因子控制正常大鼠肾脏中的肾血流动力学。
DOI: 10.1681/asn.v16875
发表时间: 1990
期刊: Journal of the American Society of Nephrology : JASN
影响因子: --
作者:
Baylis,C;Harton,P;Engels,K
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DOI: 10.1161/01.hyp.22.4.535
发表时间: 1993-10
期刊: Hypertension
影响因子: 8.3
作者:
D. S. Majid;A. Williams;P. Kadowitz;L. Navar
通讯作者: D. S. Majid;A. Williams;P. Kadowitz;L. Navar
DOI: 10.1152/ajprenal.1992.262.5.f718
发表时间: 1992
期刊: The American journal of physiology
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作者:
Salom,MG;Lahera,V;Miranda-Guardiola,F;Romero,JC
通讯作者: Romero,JC
离体微灌注兔传入小动脉中内皮衍生舒张因子对血管紧张素 II 诱导的血管收缩的调节。
DOI: 10.1172/jci115181
发表时间: 1991
期刊: The Journal of clinical investigation
影响因子: --
作者:
Ito,S;Johnson,CS;Carretero,OA
通讯作者: Carretero,OA
急性内皮源性舒张因子阻断的肾效应不是由血管紧张素 II 介导的。
DOI: 10.1152/ajprenal.1993.264.1.f74
发表时间: 1993
期刊: The American journal of physiology
影响因子: --
作者:
Baylis,C;Engels,K;Samsell,L;Harton,P
通讯作者: Harton,P