Klair S S, Louttit J B, Charlton P A
Biochemistry Department, Glaxo Group Research Limited, Greenford, Middlesex, England.
Life Sci. 1989;45(25):2477-83. doi: 10.1016/0024-3205(89)90014-3.
Removal of exogenously administered rat ANF (99-126) (rANF) from the rabbit coronary vasculature was investigated. Rabbit hearts were perfused using a modified Langendorff technique and ANF concentrations in the perfusate were measured by a radio-receptor assay. Under these conditions no major degradation of ANF was observed. On perfusion, however, the heart liberated large amounts of ANF. This release peaked 15 minutes after the initiation of perfusion, (685 + 220 pM) and then fell to a sustained basal level (305 + 80 pM) after 45 minutes. Although an increase in the perfusate flow rate reduced the ANF concentration, there was no significant difference in the rate of ANF release between the two flow rates used. After momentary cessation of flow ANF concentration fell to a significantly lower level, however, once again no significant change in rate of release occurred. These results suggest that the heart is not a major site of ANF degradation and that alterations in flow rate through the coronary vascular bed can cause changes in amounts of ANF released.
研究了兔冠状动脉血管对外源性给予的大鼠心房钠尿肽（99 - 126）（rANF）的清除情况。采用改良的Langendorff技术灌注兔心脏，并通过放射受体分析法测量灌注液中的ANF浓度。在这些条件下，未观察到ANF的主要降解。然而，在灌注时，心脏释放出大量的ANF。这种释放在灌注开始后15分钟达到峰值（685 + 220 pM），然后在45分钟后降至持续的基础水平（305 + 80 pM）。尽管灌注液流速的增加降低了ANF浓度，但在所使用的两种流速之间，ANF释放速率没有显著差异。在短暂停止流动后，ANF浓度降至显著更低的水平，然而，释放速率再次没有显著变化。这些结果表明，心脏不是ANF降解的主要部位，并且通过冠状血管床的流速改变可导致ANF释放量的变化。
