Allen D E, Gellai M
Am J Physiol. 1987 Mar;252(3 Pt 2):R610-6. doi: 10.1152/ajpregu.1987.252.3.R610.
The hemodynamic and renal excretory responses to 150-min atriopeptin II (AP II) infusion (330 ng X kg-1 X min-1) were assessed in five chronically instrumented rats with (FR protocol) and without (NR protocol) replaced urinary fluid losses. The observed changes were compared with those obtained by vehicle in the same rats. The hypotension seen with AP II infusion (120-min value: -27 +/- 2%, FR and NR responses combined) was due solely to a decreased cardiac output (CO; 120-min combined value: -34 +/- 3%). Total peripheral resistance remained unchanged or slightly elevated. A drop in stroke volume plus a later-developing (by 75-90 min) decrease in heart rate contributed to the CO decline. This latter bradycardic component, the opposite response to that typically produced reflexly by hypotension, was reversed by atropine sulfate treatment at 120 min and may thus be neural in origin. The finding of similar hemodynamic changes in the FR and NR rats and the lack of a significant effect of AP II on hematocrit suggest that volume depletion or a plasma extravasation were not contributors to the cardioinhibitory effect of the peptide.
在五只长期植入仪器的大鼠中，评估了在有（FR方案）和无（NR方案）尿液损失替代情况下，持续150分钟输注心房肽II（AP II，330 ng·kg⁻¹·min⁻¹）时的血流动力学和肾脏排泄反应。将观察到的变化与同一大鼠中给予赋形剂时获得的变化进行比较。输注AP II时出现的低血压（120分钟时的值：-27±2%，FR和NR反应合并）完全是由于心输出量（CO）降低（120分钟时的合并值：-34±3%）。总外周阻力保持不变或略有升高。每搏输出量下降加上后期（75 - 90分钟）心率降低导致了心输出量下降。后一种心动过缓成分，与低血压通常反射性产生的反应相反，在120分钟时经硫酸阿托品治疗后逆转，因此可能起源于神经。在FR和NR大鼠中发现相似的血流动力学变化以及AP II对血细胞比容无显著影响，表明容量耗竭或血浆外渗不是该肽心脏抑制作用的原因。
