Hironaga K, Hirooka Y, Matsuo I, Shihara M, Tagawa T, Harasawa Y, Takeshita A
Research Institute of Angiocardiology and Cardiovascular Clinic, Kyushu University School of Medicine, Fukuoka, Japan.
Hypertension. 1998 Jan;31(1):27-31. doi: 10.1161/01.hyp.31.1.27.
It has been shown that nitric oxide in the brain stem plays an important role in the control of sympathetic nerve activity. We examined the role of endogenous nitric oxide in the brain stem in the rapid central adaptation of baroreflex control of sympathetic nerve activity in anesthetized rabbits. Bilateral carotid sinuses were isolated, and a stepwise increase in pressure of 25 or 50 mm Hg for 50 to 60 seconds was applied to the carotid sinuses while the arterial pressure and renal sympathetic nerve activity were recorded. The renal sympathetic nerve activity was inhibited by the stepwise increase in carotid sinus pressure, but thereafter it gradually returned toward the baseline level despite the fact that carotid sinus pressure was kept constant. This procedure was performed after intracisternal injection of N(omega)-nitro-L-arginine methyl ester (L-NAME, 8 micromol), N(omega)-nitro-D-arginine methyl ester (D-NAME, 8 micromol), L-arginine (40 micromol), or the vehicle solution. The magnitude of the immediate and maximal inhibition of renal sympathetic nerve activity caused by a stepwise increase in carotid sinus pressure was similar between the vehicle and L-NAME treatment, but the rate of recovery of the renal sympathetic nerve activity after immediate inhibition was faster after L-NAME than after vehicle. L-Arginine reversed the effects of L-NAME. However, D-NAME or L-arginine alone had no such effects on the rate of recovery of the nerve activity. These results thus suggest that endogenous nitric oxide in the brain stem attenuates rapid adaptation of the arterial baroreflex control of the sympathetic nerve activity in rabbits.
已表明脑干中的一氧化氮在交感神经活动的控制中起重要作用。我们研究了脑干中内源性一氧化氮在麻醉兔交感神经活动的压力感受性反射控制的快速中枢适应性中的作用。分离双侧颈动脉窦,在记录动脉血压和肾交感神经活动的同时,对颈动脉窦施加25或50 mmHg的逐步压力增加,持续50至60秒。肾交感神经活动被颈动脉窦压力的逐步增加所抑制,但此后尽管颈动脉窦压力保持恒定,它仍逐渐恢复到基线水平。在脑池内注射N(ω)-硝基-L-精氨酸甲酯(L-NAME,8 μmol)、N(ω)-硝基-D-精氨酸甲酯(D-NAME,8 μmol)、L-精氨酸(40 μmol)或溶剂溶液后进行该操作。在溶剂和L-NAME处理之间,由颈动脉窦压力逐步增加引起的肾交感神经活动的即时和最大抑制程度相似,但L-NAME处理后肾交感神经活动在即时抑制后的恢复速度比溶剂处理后更快。L-精氨酸逆转了L-NAME的作用。然而,单独的D-NAME或L-精氨酸对神经活动的恢复速度没有这种影响。因此,这些结果表明脑干中的内源性一氧化氮减弱了兔交感神经活动的动脉压力感受性反射控制的快速适应性。