Possible modulation of release of atrial natriuretic factor by endothelium-derived relaxing factor.
Possible modulation of release of atrial natriuretic factor by endothelium-derived relaxing factor.
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内皮源性舒张因子可能调节心房钠尿因子的释放。
DOI：
10.1152/ajpheart.1990.259.3.h982
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发表时间：
1990
期刊：
影响因子：
--
通讯作者：
Vanhoutte,PM
中科院分区：
文献类型：
--
作者：
Sanchez-Ferrer,CF;BurnettJr,JC;Lorenz,RR;Vanhoutte,PM
本研究旨在观察内皮依赖性舒张因子抑制剂对离体大鼠心房释放心钠素的影响。电刺激的组织产生的频率依赖性增加分泌的心房肽从基础水平。皂苷（0.3mg/ml，45分钟）增强肽的基础释放。亚甲蓝（10（-5）M）、氧合血红蛋白（10（-6）M）或对苯二酚（10（-5）M）是通过不同机制抑制内皮源性舒张因子作用的药物，可引起心房利钠因子基础分泌增加。用吲哚美辛（10（-5）M）阻断环氧合酶并不改变心房肽的释放，表明心房肽不受内源性前列腺素的控制。如果测试的抑制剂干扰从心房血管的内皮细胞或内皮细胞连续释放并具有与内皮源性舒张因子相同性质的因子，则可以解释这些结果。这种释放可能对心房利钠因子的分泌产生紧张性负性调节作用。
The aim of the present study was to investigate the influence of inhibitors of endothelium-dependent relaxing factor on the release of atrial natriuretic factor from isolated rat atria. Electrical stimulation of the tissue produced a frequency-dependent increase in secretion of atriopeptide from basal levels. Saponin (0.3 mg/ml for 45 min) augmented the basal release of the peptide. Methylene blue (10(-5)M), oxyhemoglobin (10(-6)M), or hydroquinone (10(-5)M), agents that inhibit the effects of endothelium-derived relaxing factor by different mechanisms, caused an increase in the basal secretion of atrial natriuretic factor. Blockade of cyclooxygenase with indomethacin (10(-5)M) did not alter the release of atriopeptide, suggesting that it is not controlled by endogenous prostaglandins. These results would be explained if the inhibitors tested were to interfere with a factor released continuously from either endocardial cells or endothelial cells of the atrial blood vessels and having the same nature as endothelium-derived relaxing factor. Such release may exert a tonic negative modulatory influence on the secretion of atrial natriuretic factor.