Barbee R W, Harrison-Bernard L M, Zimmerman R S, Trippodo N C, Frohlich E D
Division of Research, Alton Ochsner Medical Foundation, New Orleans, Louisiana 70121.
Hypertension. 1990 Jun;15(6 Pt 2):888-93. doi: 10.1161/01.hyp.15.6.888.
Reflex activation of the sympathetic nervous system may conceal direct vasodilatory actions of atrial natriuretic factor and mediate atrial natriuretic factor-induced increases in total peripheral resistance. We determined whether peripheral sympathectomy would enhance the hypotensive actions of atrial natriuretic factor and convert the increase in total peripheral resistance to peripheral vasodilation. Sympathectomized rats studied included 1) conscious rats treated with 6-hydroxydopamine alone (partially sympathectomized) and 2) conscious anephric rats sympathectomized with adrenal demedullation and 6-hydroxydopamine (totally sympathectomized), with vascular tone returned to levels of sham-operated (control) rats with norepinephrine infusion. Sympathectomized rats and appropriate control rats received rat atrial natriuretic factor infusion (0.5 microgram/kg/min) or vehicle for 1 hour. Atrial natriuretic factor infusion lowered mean arterial pressure and increased hematocrit in control rats but not in partially sympathectomized rats. Changes in cardiac output and total peripheral resistance were not significantly different between control and partially sympathectomized rats. In totally sympathectomized rats, atrial natriuretic factor lowered mean arterial pressure more than in control rats; changes in cardiac output were nearly identical in both groups, but there were no changes in total peripheral resistance from control levels in the totally sympathectomized group. Changes in plasma volume and central venous pressure were similar in totally sympathectomized rats and control rats. These findings suggest that reflex sympathetic activity largely mediated atrial natriuretic factor-induced increases in total peripheral resistance but failed to reveal an atrial natriuretic factor-mediated sustained vasodilation in the absence of sympathetic reflexes. Furthermore, atrial natriuretic factor decreased cardiac output, central venous pressure, and plasma volume independent of the sympathetic nervous system.
交感神经系统的反射性激活可能掩盖心房利钠因子的直接血管舒张作用,并介导心房利钠因子引起的总外周阻力增加。我们确定外周交感神经切除术是否会增强心房利钠因子的降压作用,并将总外周阻力的增加转化为外周血管舒张。所研究的交感神经切除大鼠包括:1)仅用6-羟基多巴胺处理的清醒大鼠(部分交感神经切除)和2)经肾上腺髓质剥脱和6-羟基多巴胺交感神经切除的清醒无肾大鼠(完全交感神经切除),通过输注去甲肾上腺素使血管张力恢复到假手术(对照)大鼠的水平。交感神经切除大鼠和适当的对照大鼠接受大鼠心房利钠因子输注(0.5微克/千克/分钟)或赋形剂,持续1小时。在对照大鼠中,输注心房利钠因子可降低平均动脉压并增加血细胞比容,但在部分交感神经切除大鼠中则不然。对照大鼠和部分交感神经切除大鼠的心输出量和总外周阻力变化无显著差异。在完全交感神经切除大鼠中,心房利钠因子降低平均动脉压的程度超过对照大鼠;两组的心输出量变化几乎相同,但完全交感神经切除组的总外周阻力与对照水平相比没有变化。完全交感神经切除大鼠和对照大鼠的血浆容量和中心静脉压变化相似。这些发现表明,反射性交感神经活动在很大程度上介导了心房利钠因子引起的总外周阻力增加,但在没有交感神经反射的情况下未能揭示心房利钠因子介导的持续性血管舒张。此外,心房利钠因子降低心输出量、中心静脉压和血浆容量,与交感神经系统无关。