Hypoxia-induced release of atrial natriuretic factor (ANF) from the isolated rat and rabbit heart.

Hypoxia-induced release of atrial natriuretic factor (ANF) from the isolated rat and rabbit heart.
复制标题

缺氧诱导大鼠和兔离体心脏释放心房钠尿因子(ANF)。

DOI:
10.1016/0006-291x(86)91108-3
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发表时间:
1986
影响因子:
3.1
通讯作者:
Pence,RA
Pence,RA
中科院分区:
生物学4区
文献类型:
--
作者:
Baertschi,AJ;Hausmaninger,C;Walsh,RS;MentzerJr,RM;Wyatt,DA;Pence,RA

文献摘要

被引文献

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在离体大鼠和家兔心脏上,观察了低氧对心钠素(ANF)释放的影响。将流出物样品冷冻,等待提取和ANF的放射免疫测定。缺氧(10分钟)引起的3.9倍(大鼠)和4.6倍(兔)的心钠素释放增加超过对照值。ANF释放在复氧后8-11分钟内恢复到对照水平。长时间(20分钟)缺氧诱发进一步心钠素释放。心钠素释放的增加以及心室压、心率和冠状动脉灌注压的降低是完全可逆的,表明组织没有受损。这些结果表明,缺氧诱导大量释放的心钠素的机制尚未解释。
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.