Macula densa derived nitric oxide in regulation of glomerular capillary pressure.

Macula densa derived nitric oxide in regulation of glomerular capillary pressure.
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致密斑衍生的一氧化氮调节肾小球毛细血管压力。

DOI:
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发表时间:
1996
影响因子:
19.6
通讯作者:
G. Persson
G. Persson
中科院分区:
医学1区
文献类型:
--
作者:
C. Thorup;A. Erik;G. Persson

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一氧化氮(NO)是由一氧化氮合酶(NOS)产生的。在肾脏中至少发现了三种不同的NOS亚型。本研究通过对麻醉大鼠小管肾小球反馈(TGF)机制的研究,探讨选择性抑制诱导型亚型(iNOS)和神经元型亚型(bNOS)对肾小球毛细血管压力(PGC)的影响。通过人工超滤液(包括载药剂、NOS抑制剂或l -精氨酸)改变Henle灌注率环,测量近端管止流压力(PSF),估计TGF系统激活后PGC的变化。输注非特异性NOS抑制剂(N - ω -硝基- l -精氨酸)使最大TGF反应(δ PSF)增加84%,l -精氨酸使δ PSF降低37%。选择性inos抑制剂氨基胍不能增加δ PSF,而非特异性NOS抑制剂甲基胍可使δ PSF增加64%。7-硝基吲哚唑(7-NI)是一种选择性bNOS抑制剂,经管内注射可使δ PSF增加57%,腹腔注射7-NI可使δ PSF增加78%,血压无变化。由于bNOS只存在于黄斑致密(macula densa, MD)细胞中,这些结果证实并强化了MD产生的NO在调控TGF和PGC中的强制性作用,这是之前提出的。在肾脏中广泛表达的iNOS似乎在PGC的调节中没有任何重要作用。
Nitric oxide (NO) is produced by enzymes called nitric oxide synthases (NOS). At least three different isoforms of NOS have been identified in the kidney. This study examines the effects of selective inhibition of the inducible isoform (iNOS) and the neuronal isoform (bNOS) on the glomerular capillary pressure (PGC), through studies of the tubuloglomerular feedback (TGF) mechanism in anaesthetized rats. The proximal tubular stop-flow pressure (PSF) was measured to estimate changes in PGC obtained after activation of the TGF system by varying the loop of Henle perfusion rate with artificial ultrafiltrate including vehicle, NOS inhibition or L-arginine. Infusion of nonspecific NOS inhibition (N omega-Nitro-L-arginine) increased maximal TGF responses (delta PSF) by 84% and L-arginine decreased delta PSF by 37%. Aminoguanidine, a selective iNOS-inhibitor, failed to increase delta PSF, whereas the nonspecific NOS inhibitor methylguanidine increased delta PSF by 64%. 7-Nitro indazole (7-NI), a selective bNOS inhibitor, increased delta PSF by 57% when infused intratubularly, and intraperitoneal administration of 7-NI increased delta PSF by 78%, without any change in blood pressure. Since bNOS is exclusively located in the macula densa (MD) cells, these results confirm and strengthen the obligatory role of MD-produced NO in regulation of TGF and PGC, which has been suggested earlier. iNOS, widely expressed in the kidney, does not seem to play any important role in regulation of PGC.
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影响因子: --
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