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首页> 外文期刊>Life sciences >In vivo effects of the controlled NO donor/scavenger ruthenium cyclam complexes on blood pressure.
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In vivo effects of the controlled NO donor/scavenger ruthenium cyclam complexes on blood pressure.

机译：受控的NO供体/清除剂钌cyclam复合物对血压的体内影响。

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摘要

Ruthenium(II/III) complexes able to bind and release NO* were tested in vivo, in conscious Wistar rats instrumented for continuous blood pressure (BP) measurement and administration of in bolus injections (5 to 100 nmol/Kg i.v.) of trans-[Ru(II)Cl(NO+)(cyclam)](PF6)2 (cyclam-NO) or sodium nitroprusside (SNP). For normotensive rats, cyclam-NO produced a sustained 10% BP reduction of basal MAP during 7 +/- 0.4 to 11 +/- 0.3 min. In acute hypertensive rats, cyclam-NO produced BP reduction 3-fold larger than in normotensive rats and similar to that of SNP (maximal effect: 41 +/- 1.3 vs. 45 +/- 2.2 mmHg, respectively). However, the duration of the effect of cyclam-NO was 13 to 21-fold longer than that of SNP. The hypotensive effect of cyclam-NO was fully blocked in presence of continuous infusion of a NO* scavenger, carboxy-PTIO (6 mmol/Kg/min), or of the inhibitor of cGMP activation, methylene blue (83 nmol/Kg/min), or of the cyclam-NO precursor, trans-[RuCl(tfins)(cyclam)](tfms) (cyclam-tfms) (500 mmol/Kg/min). The long lasting BP reduction of cyclam-NO can be interpreted in terms of a slower rate of NO* release (k-NO = 2.2 x 10(-3) S(-1) at 35 degrees C) following chemical reduction (E(0') = 0.10 V vs NHE). In summary, cyclam-NO showed an hypotensive effect around 20 times longer than SNP in either normotensive or hypertensive rats, which was completely inhibited by methylene blue or carboxy-PTIO. Continuous infusion of cyclam-tfms completely blocked the hypotensive effect of cyclam-NO by scavenging the NO* released by the reduced cyclam-NO.
机译：在有意识的Wistar大鼠体内测试了能够结合和释放NO *的钌（II / III）配合物，该大鼠装备了连续血压（BP）测量和推注（5至100 nmol / Kg iv）反式- [Ru（II）Cl（NO +）（cyclam）]（PF6）2（cyclam-NO）或硝普钠（SNP）。对于血压正常的大鼠，在7 +/- 0.4至11 +/- 0.3分钟内，cyclam-NO可使基础MAP的血压持续降低10％。在急性高血压大鼠中，cyclam-NO产生的血压降低量比正常血压大鼠高3倍，并且与SNP相似（最大作用分别为41 +/- 1.3与45 +/- 2.2 mmHg）。但是，Cyclam-NO的作用持续时间比SNP长13到21倍。在连续注入NO *清除剂羧基-PTIO（6 mmol / Kg / min）或cGMP激活抑制剂亚甲基蓝（83 nmol / Kg / min）的情况下，完全可以阻断cyclam-NO的降压作用。 ）或cyclam-NO前体的反式-[RuCl（tfins）（cyclam）]（tfms）（cyclam-tfms）（500 mmol / Kg / min）。 Cyclam-NO的持久BP降低可解释为化学还原后（E（）（）的NO *释放速率降低（k-NO =在35摄氏度时为2.2 x 10（-3）S（-1））。 0'）= 0.10 V对NHE）。总之，在正常血压或高血压大鼠中，cyclam-NO的降压作用是SNP的20倍左右，而亚甲基蓝或羧基-PTIO则完全抑制了其作用。连续输注cyclam-tfms可通过清除还原的cyclam-NO释放的NO *来完全阻断cyclam-NO的降压作用。

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