Relation between pressure natriuresis and urinary excretion of nitrate/nitrite in anesthetized dogs.
Relation between pressure natriuresis and urinary excretion of nitrate/nitrite in anesthetized dogs.
复制标题
麻醉犬压力尿钠与尿硝酸盐/亚硝酸盐排泄之间的关系。
DOI：
10.1161/01.hyp.25.4.860
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发表时间：
1995
期刊：
影响因子：
--
通讯作者：
Navar,LG
中科院分区：
文献类型：
--
作者：
Majid,DS;Godfrey,M;Grisham,MB;Navar,LG
肾动脉压（RAP）变化期间肾内一氧化氮（NO）形成的变化被认为是介导压力尿钠排泄的机制。为了进一步检验这一假设，我们在麻醉钠充足的狗中，在肾内输注NO合成抑制剂硝基-l-精氨酸（NLA；50 μg·kg−1·min−1）之前（n=9）和期间（n=6）检查了RAP与硝酸盐/亚硝酸盐（NO3−/NO2−；NO代谢物）尿排泄率之间的关系。将样品中的 NO3− 酶促还原为 NO2− 后，通过格里斯反应和分光光度法测量尿液中 NO3−/NO2− 浓度。在控制条件下，尿NO3−/NO2−排泄率随着RAP的降低而下降（150至75 mm Hg；斜率，0.04±0.01 nmol·min−1·g−1·mm Hg−1），并与尿钠排泄（UNaV）减少相关。 NO3−/NO2−排泄率的变化与 RAP (r=.48;P<.005) 或 UNaV (r=.59;P<.001) 的变化呈正相关。 NLA输注导致NO3−/NO2−排泄率下降（4.8±1.4至1.0±0.3 nmol·min−1·g−1），并与UNaV（4.3±0.3至0.7±0.2 μL·min−1·g−1）、钠排泄分数（2.9±0.2%至0.5±0.1%）和肾血减少相关。流量（4.8±0.3 至 3.3±0.2 mL·min−1·g−1），肾小球滤过率没有变化。此外，在 NO 合成抑制期间，NO3−/NO2− 和钠排泄反应对 RAP 变化的反应显着减弱。在另外四只狗中，观察到在给予噻嗪类和阿米洛利利尿剂期间，尿NO3-/NO2-排泄率没有变化，这表明NO3-/NO2-排泄对RAP变化的反应不仅仅是由于尿流率或钠排泄的变化。这些发现与 RAP 急性变化期间，肾内 NO 生成速率的变化可能是钠排泄变化的原因一致。
Alterations in intrarenal nitric oxide (NO) formation during changes in renal arterial pressure (RAP) have been suggested as a mechanism mediating pressure natriuresis. To test this hypothesis further, we examined the relation between RAP and the urinary excretion rate of nitrate/nitrite (NO3−/NO2−; NO metabolites) in anesthetized sodium-replete dogs before (n=9) and during (n=6) intrarenal infusion of the NO synthesis inhibitor nitro-l-arginine (NLA; 50 μg · kg−1· min−1). Urinary NO3−/NO2−concentrations were measured with the Griess reaction and spectrophotometry methods after enzymatic reduction of NO3−to NO2−in the samples. During control conditions, there were decreases in the urinary NO3−/NO2−excretion rate in response to reductions in RAP (150 to 75 mm Hg; slope, 0.04±0.01 nmol · min−1· g−1· mm Hg−1) in association with decreases in urinary sodium excretion (UNaV). There was a positive correlation between changes in NO3−/NO2−excretion rate and changes in RAP (r=.48;P<.005) or UNaV (r=.59;P<.001). NLA infusion resulted in decreases in NO3−/NO2−excretion rate (4.8±1.4 to 1.0±0.3 nmol · min−1· g−1) in association with reductions in UNaV (4.3±0.3 to 0.7±0.2 μL · min−1· g−1), fractional excretion of sodium (2.9±0.2% to 0.5±0.1%), and renal blood flow (4.8±0.3 to 3.3±0.2 mL · min−1· g−1), without changes in glomerular filtration rate. Furthermore, there was a marked attenuation of the NO3−/NO2−and sodium excretory responses to alterations in RAP during NO synthesis inhibition. In another four dogs, it was observed that urinary NO3−/NO2−excretion rate did not change during administration of thiazide and amiloride diuretics, indicating that the NO3−/NO2−excretory responses to alterations in RAP were not simply due to changes in urine flow rate or sodium excretion. These findings are consistent with the hypothesis that during acute changes in RAP, intrarenal changes in NO production rate may be responsible for the changes in sodium excretion.