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目的：探讨诱导型一氧化氮合酶在血液动力学调控中的作用。方法：本实验所用动物为健康、雄性、Ｄａｈｌ盐敏感（ＤＳ）及 Ｄａｈｌ盐不敏感（ＤＲ）大鼠，体重（１９０±４）ｇ。通过慢性血液动力学实验观察静脉输入诱导型一氧化氮合酶（ｉＮＯＳ）抑制剂ＡＧ对大鼠平均动脉压的影响。此外，本实验还测定了一氧化氮（ＮＯ）终产物ＮＯ２－及ＮＯ３－含量以及钙依赖及钙不依赖的ＮＯＳ活性以了解ｉＮＯＳ的功能。结果：（１）ｉＮＯＳ特异抑制剂 ＡＧ对正常血压（包括高盐或低盐输入的Ｄａｈｌ盐抵抗大鼠及低盐输入的Ｄａｈｌ盐敏感大鼠）没有明显影响，但能明显放大高钠引起的ＤＳ大鼠的血压上升效应；（２）高盐在导致的ＤＳ大鼠血压升高的同时，能引起ｉＮＯＳ活性的明显升高。结论：ｉＮＯＳ是参与血液动力学调控的重要组成部分，尤其是在血压处于较高水平时，ｉＮＯＳ具有不容忽视的调节作用。
Objective: To investigate the role of inducible nitric oxide synthase in hemodynamic regulation. Methods: The animals used in this experiment were healthy, male, Dahl salt sensitive (DS) and Dahl salt insensitive (DR) rats weighing 190 ± 4 g. The effect of intravenous inducible nitric oxide synthase (iNOS) inhibitor AG on mean arterial pressure in rats was observed by chronic hemodynamic test. In addition, nitric oxide (NO) end products such as NO2- and NO3-, as well as calcium-dependent and calcium-independent NOS activity, were also assayed to understand the function of iNOS. Results: (1) The iNOS-specific inhibitor AG had no significant effect on normotensive blood pressure (including Dahl salt-resistant rats with high or low salt input and Dahl salt-sensitive rats with low salt input), but significantly increased the sodium-induced DS rats blood pressure effects; (2) high salt in the DS rats caused by high blood pressure at the same time, can cause a significant increase in iNOS activity. CONCLUSIONS: iNOS is an important part of hemodynamic regulation. Especially at high blood pressure, iNOS can not be neglected.