Miyano H, Kawada T, Sugimachi M, Shishido T, Sato T, Alexander J, Sunagawa K
Department of Cardiovascular Dynamics, National Cardiovascular Center Research Institute, Osaka, Japan.
Am J Physiol. 1997 Jul;273(1 Pt 2):H38-43. doi: 10.1152/ajpheart.1997.273.1.H38.
We examined whether the inhibition of nitric oxide (NO) synthesis potentiates the dynamic sympathetic regulation of the cardiovascular system through the baroreflex. In anesthetized rabbits, we imposed random pressure perturbations on the isolated carotid sinuses to evoke random changes in sympathetic nerve activity (SNA). We estimated the transfer functions from SNA to both aortic pressure (AoP) and heart rate (HR). The inhibition of NO synthesis by NG-monomethyl-L-arginine (L-NMMA, 40 mg/ kg) altered neither the transfer function from SNA to AoP nor that from SNA to HR. In contrast, sodium nitroprusside (3-6 micrograms.kg-1.min-1) significantly decreased the steady-state gain (40.3 +/- 11.7% of the control, P < 0.05) of the transfer function from SNA to AoP without affecting the HR responses. We conclude that the basal release of NO may have a role in the tonic blood pressure regulation, whereas it may not be involved in the dynamic sympathetic regulation of AoP or HR through the baroreflex.
我们研究了一氧化氮（NO）合成的抑制是否通过压力反射增强心血管系统的动态交感神经调节。在麻醉的兔子中，我们对分离的颈动脉窦施加随机压力扰动，以引起交感神经活动（SNA）的随机变化。我们估计了从SNA到主动脉压（AoP）和心率（HR）的传递函数。NG-单甲基-L-精氨酸（L-NMMA，40mg/kg）抑制NO合成既未改变从SNA到AoP的传递函数，也未改变从SNA到HR的传递函数。相比之下，硝普钠（3-6微克·kg-1·min-1）显著降低了从SNA到AoP的传递函数的稳态增益（对照组的40.3±11.7%，P<0.05），而不影响HR反应。我们得出结论，NO的基础释放可能在血压的紧张性调节中起作用，而它可能不参与通过压力反射对AoP或HR的动态交感神经调节。
