Nitric oxide inhibits sodium reabsorption in the isolated perfused cortical collecting duct.
Nitric oxide inhibits sodium reabsorption in the isolated perfused cortical collecting duct.
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发表时间：
1995-07
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通讯作者：
B. Stoos;N. García;J. Garvin
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作者：
B. Stoos;N. García;J. Garvin
间接证据表明，一氧化氮抑制钠重吸收的集合管，但缺乏直接证据。假设内皮源性一氧化氮通过阻断阿米洛利敏感性钠通道抑制皮质集合管中的钠通量。从用醋酸脱氧皮质酮（5 mg/大鼠i.m.）实验前5 ~ 9天。通过加入内皮细胞并通过乙酰胆碱（10（-7）M）诱导一氧化氮的释放或通过加入一氧化氮供体将一氧化氮加入系统。乙酰胆碱诱导的内皮细胞释放一氧化氮使腔-浴钠通量降低24 +/- 7%（N = 3; P < 0.05）。加入一氧化氮供体精胺NONOate（10（-5）M），使净钠通量从10.1 +/- 2.0下降到3.6 +/- 2 pmol/mm.min（N = 5; P < 0.025）。为了确保钠通量的抑制是由于一氧化氮，使用了另一种供体硝酸甘油（2 × 10（-5）M），其使钠通量降低了43%。管腔内阿米洛利（10 μ M）使净钠通量降低83%（从14.8 +/- 1.2至2.4 +/- 0.7 pmol/mm.min; N = 5; P < 0.025）。通过精胺NONOate向肾小管添加一氧化氮使细胞内钠水平降低26%（N = 6; P < 0.005）。精胺NONOate处理的肾小管的Na（+）-K+ ATP酶活性为14.7 +/- 3.2 pmol/mm.min，而对照值为10.2 +/- 2.0 pmol/mm. min。硝酸甘油也不显著影响泵活性。（250字处删节）
Indirect evidence suggests that nitric oxide inhibits sodium reabsorption by the collecting duct; however, direct evidence is lacking. It was hypothesized that endothelium-derived nitric oxide inhibits sodium flux in the cortical collecting duct by blocking amiloride-sensitive sodium channels. Tubules were obtained from Sprague-Dawley rats pretreated with deoxycorticosterone acetate (5 mg/rat i.m.) 5 to 9 days before the experiment. Nitric oxide was added to the system by either the addition of endothelial cells and the induction of the release of nitric oxide via acetylcholine (10(-7) M) or by the addition of nitric oxide donors. Acetylcholine-induced nitric oxide release from endothelial cells decreased lumen-to-bath sodium flux by 24 +/- 7% (N = 3; P < 0.05). The addition of the nitric oxide donor, spermine NONOate (10(-5) M), decreased net sodium flux 68% from 10.1 +/- 2.0 to 3.6 +/- 2 pmol/mm.min (N = 5; P < 0.025). To assure that the inhibition of sodium flux was due to nitric oxide, another donor, nitroglycerin (2 x 10(-5) M), was used, which decreased sodium flux by 43%. Luminal amiloride (10 microM) decreased net sodium flux by 83% (from 14.8 +/- 1.2 to 2.4 +/- 0.7 pmol/mm.min; N = 5; P < 0.025). The addition of nitric oxide via spermine NONOate to tubules decreased intracellular sodium levels by 26% (N = 6; P < 0.005). The Na(+)-K+ATPase activity of spermine NONOate-treated tubules was 14.7 +/- 3.2 pmol/mm.min compared with the control value of 10.2 +/- 2.0 pmol/mm.min. Nitroglycerin did not significantly affect pump activity either.(ABSTRACT TRUNCATED AT 250 WORDS)