Baertschi A J, Hausmaninger C, Walsh R S, Mentzer R M, Wyatt D A, Pence R A
Biochem Biophys Res Commun. 1986 Oct 15;140(1):427-33. doi: 10.1016/0006-291x(86)91108-3.
The effect of hypoxia on the release of atrial natriuretic factor (ANF) was studied in isolated, constant-flow perfused hearts of rats and rabbits. Effluent samples were frozen pending extraction and radioimmunoassay of ANF. Hypoxia (10 min) caused a 3.9-fold (rats) and 4.6-fold (rabbits) increase of ANF release over control values. ANF release returned to control levels within 8-11 min of reoxygenation. Prolonged (20 min) hypoxia evoked further ANF release. The increase in ANF release and decrease in ventricular pressure, heart rate and coronary perfusion pressure were fully reversible, suggesting that tissues were not damaged. These results demonstrate that hypoxia induces a massive release of ANF by an as yet unexplained mechanism.
在大鼠和家兔的离体恒流灌注心脏中研究了缺氧对心房利钠因子（ANF）释放的影响。流出液样本在提取和进行ANF放射免疫测定之前进行冷冻。缺氧（10分钟）导致ANF释放量比对照值增加了3.9倍（大鼠）和4.6倍（家兔）。复氧8 - 11分钟内，ANF释放量恢复到对照水平。长时间（20分钟）缺氧引起ANF进一步释放。ANF释放量的增加以及心室压力、心率和冠状动脉灌注压力的降低是完全可逆的，这表明组织未受损。这些结果表明，缺氧通过一种尚未明确的机制诱导ANF大量释放。
