Pegram B L, Trippodo N C, Natsume T, Kardon M B, Frohlich E D, Cole F E, MacPhee A A
Fed Proc. 1986 Aug;45(9):2382-6.
The atrial natriuretic hormone (ANH) alters cardiovascular function independent of changes in body fluid volume. Most investigators agree that ANH decreases mean arterial pressure (MAP). However, although some investigators have observed a decrease in total peripheral resistance in association with the decrease in MAP, a more frequent observation has been decreased cardiac output (CO). The mechanism whereby ANH decreases CO is unknown, but does not appear to be the result of direct myocardial depression, reductions in intravascular or cardiopulmonary volumes, or venodilation. Alterations in skeletal muscle and splanchnic blood flow have been reported by some but not all investigators. Although increases in renal blood flow have been reported, they are transitory and have not been consistently observed by all researchers. The cardiovascular effects of ANH appear to be influenced not only by the dose, but also by the cardiovascular control mechanisms that operate at the time of ANH administration. Non-renin-dependent hypertensive models exhibit a decrease in MAP associated with decreased CO, whereas in renin-dependent animals this hypotension is associated with a decrease in total peripheral resistance.
心房利钠肽（ANH）可独立于体液容量变化而改变心血管功能。大多数研究人员一致认为，ANH可降低平均动脉压（MAP）。然而，尽管一些研究人员观察到总外周阻力随MAP降低而下降，但更常见的观察结果是心输出量（CO）降低。ANH降低CO的机制尚不清楚，但似乎不是直接心肌抑制、血管内或心肺容量减少或静脉扩张的结果。一些但并非所有研究人员都报告了骨骼肌和内脏血流的改变。尽管有报告称肾血流量增加，但这些增加是短暂的，并非所有研究人员都一致观察到。ANH的心血管效应似乎不仅受剂量影响，还受ANH给药时运行的心血管控制机制影响。非肾素依赖性高血压模型表现出MAP降低且CO降低，而在肾素依赖性动物中，这种低血压与总外周阻力降低有关。
