抑制一氧化氮合酶对大鼠主动脉血管紧张素Ⅱ受体的影响

The inhibition of nitric oxide synthase for long time up-regulates vascular angiotensin Ⅱ receptor

目的：本文应用ＮＯ合酶（ＮＯＳ）竞争性抑制剂左旋硝基精氨酸（Ｌ－ＮＮＡ）诱导大鼠高血压，观察对主动脉血管紧张素Ⅱ（ＡｎｇⅡ）和ＡｎｇⅡ受体的影响。方法：采用腹腔注射Ｌ－ＮＮＡ复制大鼠高血压模型，分别用放射免疫法测定主动脉ＡｎｇⅡ、放射配基结合法测定主动脉组织ＡｎｇⅡ受体和Ｇｒｉｅｓｓ法测定血浆ＮＯｘ含量。结果：Ｌ－ＮＮＡ使大鼠血压明显高于对照组（＋１４２％，Ｐ＜０．０１），４周组心系数高１２８‰（Ｐ＜０．０１），血浆ＮＯｘ水平低于对照组４８％，血浆ＡｎｇⅡ水平无明显差异；血管组织ＡｎｇⅡ含量４周组显著高６１２％（Ｐ＜０．０１），且４周组［１２５Ｉ］－ＡｎｇⅡ最大结合能力（Ｂｍａｘ）高６倍（Ｐ＜０．０１），亲和力（Ｋｄ）高１倍（Ｐ＜０．０１）。结论：抑制ＮＯＳ诱导高血压主要是通过局部组织肾素－血管紧张素系统（ＲＡＳ）发挥作用的，长期慢性抑制 ＮＯＳ可使血管组织 ＡｎｇⅡ水平升高并导致血管ＡｎｇⅡ受体上调，此结果为“ＮＯＳ抑制诱发ＡｎｇⅡ依赖型高血压”假说提供新的依据。

AIM: To observe the effects of aortal angiotensin Ⅱ (Ang Ⅱ )levels and AngⅡ receptor in the hy- pertensive rat models. METHODS: Intraperinoneal injection of L - Nw - nitro-arginine (L - NNA) into rats induced hypertensive model, the binding of aortal Ang Ⅱ receptor and the contents of aortal tissue Aug Ⅱ and plasma NO2-+ NO3- (NOx) were determined. RESULTS: Compared with the control group, the bind pressure of the rats treated with L - NNA was significantly increased by 142% (P < 0.01 ), the plasma NOx levels were decreased by 48%. However, in the rats treated for 4 weeks the ratio of cudal index was increased by 128% (P < 0. 01 ), the plasma Ang Ⅱ levels weren' t significantly changed, the contents of vascular tissue Aug Ⅱ were increased by 612% (P<0.01) and the Bmax of [125I] - Aug Ⅱ was increased by sir bines (P < 0.01), the sanity was doubled respec- tively. CONCLUSIONS: Nitric oxide synthase (NOS) inhibition mostly influes the reninangiotensin system in regional tissue. The inhibition for long the up - regulates vascular Aug Ⅱ and Aug Ⅱ receptor, which can support the hy- pothesis 'NOS inhibition can induce Ang Ⅱ - depended hpertension'.