内源性和外源性NO对大鼠动脉压力感受器反射的调节

目的研究内源性和外源性一氧化氮(NO)对动脉压力感受器反射的不同作用.方法静脉注射苯肾上腺素(PE, 30 μg·kg-1),改变大鼠血压,诱发动脉压力感受器反射.分别静脉注射硝普钠(SNP,10.2 μg·kg-1)和L-精氨酸(L-Arg, 25 mg·kg-1)以产生外源性和内源性NO,静脉注射L-NAME(10mg ·kg-1)抑制内源性NO的产生,并估测NO的产生或抑制对压力感受器敏感性的影响.结果与正常状态比较,L-Arg使大鼠压力感受器反射敏感性(Gmax)和血压-心率拟合曲线斜率τ显著下降[Gmax=-1.469±0.120beats/(min·mmHg) vs. -0.664±0.080 beats/(min·mmHg), P<0.01;τ=0.086豹0.005vs. 0.049±0.007, P<0.05].SNP尽管也引起了上述参数的减小,但作用不显著.与L-Arg和SNP的作用相反,L-NAME导致了Gmax和τ的上升,但变化不显著.结论内源性和外源性NO对压力感受器反射的作用不同,内源性NO可能抑制压力感受器反射的敏感性.

Modulation of Baroreflex Activity by Exogenous and Endogenous NO in SD Rats

Objective To assess the modulation of baroreflex activity by exogenous and endogenous nitric oxide (NO) in SD rats. Method The normal baroreflex sensitivity of SD rat was evaluated by intravenous (I.v.) administration of Phenylephrine (PE, 30 μg·kg-1) to elevate blood pressure. Exogenous and endogenous nitric oxide (NO) were respectively produced by I.v. Infusion of sodium nitroprusside (SNP, 10.2 μg·kg-1) and L-arginine (L-Arg, 25 mg·kg-1). And NG-nitro-L-arginine methylester (L-NAME, 10 mg·kg-1) was infused to inhibit the generation of NO. Meanwhile, baroreflex sensitivity fluctuations caused by PE were estimated. Result Compared with the normal state, L-Arg significantly reduced the baroreflex sensitivity (Gmax) and the slope coefficient τ of the blood pressure-heart rate curve [Gmax=-1.469±0.120 beats/(min·mmHg) vs. -0.664±0.080 beats/(min·mmHg), P<0.01; τ=0.0860.005 vs. 0.0490.007, P<0.05]. SNP also led to attenuation of Gmax and τ [Gmax=-1.277±0.392 beats/(min·mmHg) vs. -0.943±0.297 beats/(min·mmHg); τ=0.074豹0.027 vs. 0.071±0.023] but the changes were not significant. In contrast to L-Arg and SNP, L-NAME induced raise of Gmax and τ [Gmax=-0.705±0.231 beats/(min·mmHg) vs. -1.065±0.200 beats/(min·mmHg); τ=0.0450.011 vs. 0.0590.026], however, they were statistically insignificant. Conclusion The results demonstrated that NO imposes effect on baroreflex activity, and the behaviors of exogenous and endogenous NO are different. Endogenous NO may be involved in the regulation of autonomic nervous system via central nervous system or carotid sinus, and inhibits the baroreflex sensitivity.