Atriopeptin II elevates cyclic GMP, activates cyclic GMP-dependent protein kinase and causes relaxation in rat thoracic aorta.
Atriopeptin II elevates cyclic GMP, activates cyclic GMP-dependent protein kinase and causes relaxation in rat thoracic aorta.
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Atriopeptin II 升高环 GMP，激活环 GMP 依赖性蛋白激酶并导致大鼠胸主动脉松弛。
DOI：
10.1016/0167-4889(85)90124-7
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发表时间：
1985
期刊：
影响因子：
--
通讯作者：
Murad,F
中科院分区：
文献类型：
--
作者：
Fiscus,RR;Rapoport,RM;Waldman,SA;Murad,F
合成心房肽II，一种心钠素与强大的血管舒张作用，研究了在大鼠胸主动脉的隔离条，以确定其对收缩力，环核苷酸浓度和内源性活性的环核苷酸依赖性蛋白激酶的行动。无论内皮层是否存在，心房肽II均能舒张用0.3 μM去甲肾上腺素预收缩的主动脉条。心房肽素II的舒张作用与环GMP浓度的增加和环GMP依赖性蛋白激酶（环GMP激酶）的激活密切相关，呈时间和浓度依赖性。所有三种效应的阈值浓度均为1 nM。心房肽II（10 nM，10分钟）产生80%的松弛，环GMP浓度增加8倍，环GMP-激酶活性比增加2倍。心房肽II没有显着改变环AMP浓度或环AMP依赖性蛋白激酶活性。这些数据表明，环GMP和环GMP-激酶可能介导血管舒张一类新的血管活性剂，心房利钠因子。类似的效果已经观察到与硝基血管扩张剂，硝普钠，和内皮依赖性血管扩张剂，乙酰胆碱。因此，一个共同的生化作用机制，包括环GMP的积累和激活环GMP-激酶可能参与血管舒张硝基血管扩张剂，内皮依赖性血管扩张剂和心房利钠因子。
Synthetic atriopeptin II, an atrial natriuretic factor with potent vasodilatory effects, was studied in isolated strips of rat thoracic aorta to determine its actions on contractility, cyclic nucleotide concentrations and endogenous activity of cyclic nucleotide-dependent protein kinases. Atriopeptin II was found to relax aortic strips precontracted with 0.3 μM norepinephrine whether or not the endothelial layer was present. Relaxation to atriopeptin II was closely correlated in a time- and concentration-dependent manner with increases in cyclic GMP concentrations and activation of cyclic GMP-dependent protein kinase (cyclic GMP-kinase). The threshold concentration for all three effects was 1 nM. Atriopeptin II (10 nM for 10 min) produced an 80% relaxation, an 8-fold increase in cyclic GMP concentrations and a 2-fold increase in cyclic GMP-kinase activity ratios. Atriopeptin II did not significantly alter cyclic AMP concentrations or cyclic AMP-dependent protein kinase activity. These data suggest that cyclic GMP and cyclic GMP-kinase may mediate vascular relaxation to a new class of vasoactive agents, the atrial natriuretic factors. Similar effects have been observed with the nitrovasodilator, sodium nitroprusside, and the endothelium-dependent vasodilator, acetylcholine. Therefore, a common biochemical mechanism of action that includes cyclic GMP accumulation and activation of cyclic GMP-kinase may be involved in vascular relaxation to nitrovasodilators, endothelium-dependent vasodilators and atrial natriuretic factors.