Fujisawa Y, Mori N, Yube K, Miyanaka H, Miyatake A, Abe Y
Research Equipment Center, Kagawa Medical University, Kagawa 761-0793, Japan.
Am J Physiol. 1999 Jul;277(1):H8-14. doi: 10.1152/ajpheart.1999.277.1.H8.
The effect of inhibition of nitric oxide (NO) synthesis on the responses of blood pressure (BP), heart rate (HR), and renal sympathetic nerve activity (RSNA) during hemorrhaging was examined with the use of an NO synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), in conscious rats. In the 0.9% saline group, hemorrhage (10 ml/kg body wt) did not alter BP but significantly increased HR and RSNA by 88 +/- 12 beats/min and 67 +/- 12%, respectively. Intravenous infusion of L-NAME (50 microg. kg(-1). min(-1)) significantly attenuated these tachycardic and sympathoexcitatory responses to hemorrhage (14 +/- 7 beats/min and 26 +/- 12%, respectively). Pretreatment of L-arginine (87 mg/kg) recovered the attenuation of HR and RSNA responses induced by L-NAME (92 +/- 6 beats/min and 64 +/- 10%, respectively). L-NAME by itself did not alter the baroreceptor reflex control of HR and RSNA. Hemorrhage increased the plasma vasopressin concentration, and its increment in the L-NAME-treated group was significantly higher than that in the 0.9% saline group. Pretreatment with the vascular arginine vasopressin V(1)-receptor antagonist OPC-21268 (5 mg/kg) recovered the attenuation of RSNA response induced by L-NAME (54 +/- 7%). These results indicate that NO modulated HR and RSNA responses to hemorrhage but did not directly affect the baroreceptor reflex arch. It can be assumed that NO modulated the baroreflex function by altering the secretion of vasopressin induced by hemorrhage.
利用一氧化氮合酶抑制剂N(G)-硝基-L-精氨酸甲酯（L-NAME），在清醒大鼠中研究了抑制一氧化氮（NO）合成对出血期间血压（BP）、心率（HR）和肾交感神经活动（RSNA）反应的影响。在0.9%生理盐水组中，出血（10 ml/kg体重）未改变血压，但显著增加心率和肾交感神经活动，分别增加88±12次/分钟和67±12%。静脉输注L-NAME（50μg·kg(-1)·min(-1)）显著减弱了这些对出血的心动过速和交感兴奋反应（分别为14±7次/分钟和26±12%）。L-精氨酸（87 mg/kg）预处理恢复了L-NAME诱导的心率和肾交感神经活动反应的减弱（分别为92±6次/分钟和64±10%）。L-NAME本身未改变压力感受器对心率和肾交感神经活动的反射控制。出血增加了血浆血管加压素浓度，L-NAME治疗组的增加幅度显著高于0.9%生理盐水组。用血管精氨酸血管加压素V(1)受体拮抗剂OPC-21268（5 mg/kg）预处理恢复了L-NAME诱导的肾交感神经活动反应的减弱（54±7%）。这些结果表明，NO调节了对出血的心率和肾交感神经活动反应，但未直接影响压力感受器反射弧。可以推测，NO通过改变出血诱导的血管加压素分泌来调节压力反射功能。
