肾髓质诱导型一氧化氮合酶在动脉血压调控中的作用(英文)

Role of renal medullary inducible nitric oxide synthase in the regulation of arterial pressure

本文通过慢性血液动力学实验 ,观察了肾髓质局部输入诱导型一氧化氮合酶 (iNOS)抑制剂AG (aminoguanidine)对Dahl盐敏感大鼠 (DS)、Dahl盐抵抗大鼠 (DR)及SD (SpragueDawley)大鼠动脉血压的影响 ,并测定了一氧化氮 (NO)代谢终产物NO2 及NO3 含量 (UNOx)、iNOS活性、肾功能以及血浆肾素活性 (PRA)。结果表明 :AG能明显放大高盐 ( 8% )引起的DS及SD大鼠的血压上升效应 ,降低DS大鼠肾小球滤过率 (GFR)、肾有效血浆流量 (ERPF)及血浆肾素活性 (PRA)。肾髓质局部输入高盐还能显著提高DS大鼠肾组织尤其是肾内髓及外髓iNOS活性。这一结果表明 。

In the present work, we have examined the effects of selective inhibition of the inducible isoform of nitric oxide syn^thase (iNOS) in rat medulla by aminoguanidine (AG) on the arterial pressure of Dahl salt sensitive (DS), Dahl salt resistant (DR) and Sprague Dawley (SD) rats by chronic in vivo hemodynamic experiment, the effect of sodium chloride (NaCl) or NaCl plus AG infusion on urinary nitrate/nitrite (urinary NO 3/NO 2,UNO x), the end product of nitric oxide (NO), excretion, glomerular filtration rate (GFR), effective renal plasma flow (ERPF) and plasma renin activity (PRA). Furthermore, an iNOS activity assay was also made. The results showed that AG infusion significantly augmented the pressor response of DS and SD rats to high NaCl (8%) intake, and decreased GFR, ERPF and PRA of DS rats. In addition, in DS rats, renal medullary interstitial administration of high NaCl significantly elevated the iNOS activity of renal tissue, especially inner medulla and outer medulla, and greatly increased UNO x excretion. Therefore, it is concluded that inducible NOS is an important modulator of blood pressure in case of NaCl induced hypertension.