Endothelium‐derived relaxing factor and atriopeptin II elevate cyclic GMP levels in pig aortic endothelial cells

Endothelium‐derived relaxing factor and atriopeptin II elevate cyclic GMP levels in pig aortic endothelial cells
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内皮源性舒张因子和心房肽 II 提高猪主动脉内皮细胞中的环 GMP 水平

DOI:
--
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发表时间:
1988
影响因子:
7.3
通讯作者:
A. Henderson
A. Henderson
中科院分区:
医学2区
文献类型:
--
作者:
W. Martin;D. G. White;A. Henderson

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1两种直接作用于可溶性鸟苷酸环化酶的刺激剂,三硝酸甘油(0.1 μm)和叠氮化钠(10 μm),以及一种受体介导的颗粒鸟苷酸环化酶刺激剂,心房肽素II(10 nm),均升高猪主动脉内皮细胞原代培养物的环GMP含量,而不影响环AMP含量。2两种受体介导的腺苷酸环化酶刺激剂胰高血糖素(1 μm)和异丙肾上腺素(10 μm)对这些细胞的cAMP或cGMP含量没有影响,但直接作用的刺激剂毛喉素(30 μm)诱导cAMP含量略有增加。3缓激肽(0.1 μm)、ATP(10 μm)和离子载体A23187(0.1 μm)三种释放内皮源性舒张因子(EDRF)的药物均能显著提高猪主动脉内皮细胞环GMP含量,而乙酰胆碱(1 μm)对EDRF无影响。这些药物对环AMP含量无任何影响。4增强EDRF作用的两种试剂:M & B 22948(100 μm)和超氧化物歧化酶(30单位ml−1),均升高猪主动脉内皮细胞的环GMP含量,而不影响环AMP含量。用过氧化氢酶(100单位ml−1)预处理细胞并不影响超氧化物歧化酶(30单位ml−1)诱导的cGMP含量的升高。5用血红蛋白(10 μm)预处理猪主动脉内皮细胞,可降低静息状态下cGMP含量,并阻断硝酸甘油引起的cGMP含量增加(0.1 μm)、叠氮化钠(10 μm)、缓激肽(0.1 μm)ATP(10 μm)、离子载体A23187(0.1 μm)、M & B 22948(100 μm)和超氧化物歧化酶(30单位ml-1),但不受心房肽素II(10 nm)诱导。6用可溶性鸟苷酸环化酶抑制剂亚甲蓝(20 μm)预处理猪主动脉内皮细胞,对静息状态下cGMP含量无影响。亚甲蓝(20 μm)可阻断硝酸甘油(0.1 μm)、M & B 22948(100 μm)和缓激肽(0.1 μm)引起的cGMP含量增加,但不能阻断心房肽素II(10 nm)引起的cGMP含量增加。7.猪主动脉内皮细胞中存在可溶性鸟苷酸环化酶、颗粒性鸟苷酸环化酶和腺苷酸环化酶。他们进一步表明,EDRF,自发产生或响应于血管活性剂,通过刺激可溶性鸟苷酸环化酶,提高内皮细胞环GMP含量。这可能是作为一个反馈回路,通过它内皮细胞调节EDRF的生产。
1 Two directly‐acting stimulants of soluble guanylate cyclase, glyceryl trinitrate (0.1 μm) and sodium azide (10 μm), and a receptor‐mediated stimulant of particulate guanylate cyclase, atriopeptin II (10 nm), each elevated the cyclic GMP content of primary cultures of pig aortic endothelial cells without affecting the cyclic AMP content. 2 Two receptor‐mediated stimulants of adenylate cyclase, glucagon (1 μm) and isoprenaline (10 μm), had no effect on the cyclic AMP or cyclic GMP content of these cells, but the directly acting stimulant, forskolin (30 μm), induced a small increase in cyclic AMP content. 3 Three agents that release endothelium‐derived relaxing factor (EDRF); bradykinin (0.1 μm), ATP (10 μm) and ionophore A23187 (0.1 μm), each markedly elevated the cyclic GMP content of pig aortic endothelial cells, but acetylcholine (1 μm) had no effect. None of these agents had any effect on cyclic AMP content. 4 Two agents that potentiate the actions of EDRF; M & B 22948 (100 μm) and superoxide dismutase (30 units ml−1), each elevated the cyclic GMP content of pig aortic endothelial cells without affecting the cyclic AMP content. Pretreating cells with catalase (100 units ml−1) did not affect the rise in cyclic GMP content induced by superoxide dismutase (30 units ml−1). 5 Pretreatment of pig aortic endothelial cells with haemoglobin (10 μm) reduced the resting content of cyclic GMP and blocked the increase in cyclic GMP content induced by glyceryl trinitrate (0.1 μm), sodium azide (10 μm), bradykinin (0.1 μm) ATP (10 μm), ionophore A23187 (0.1 μm), M & B 22948 (100 μm) and superoxide dismutase (30 units ml−1), but not that induced by atriopeptin II (10 nm). 6 Pretreatment of pig aortic endothelial cells with an inhibitor of soluble guanylate cyclase, methylene blue (20 μm), had no effect on the resting content of cyclic GMP. Methylene blue (20 μm) blocked the increase in cyclic GMP content induced by glyceryl trinitrate (0.1 μm), M & B 22948 (100 μm) and bradykinin (0.1 μm), but not that induced by atriopeptin II (10 nm). 7 The data show that soluble guanylate cyclase, particulate guanylate cyclase and adenylate cyclase are present in pig aortic endothelial cells. They further suggest that EDRF, produced spontaneously or in response to vasoactive agents, elevates endothelial cyclic GMP content by stimulating soluble guanylate cyclase. It is possible that this may serve as a feedback loop by which the endothelial cell modulates EDRF production.
心房钠尿因子引起内皮依赖性松弛并激活血管平滑肌中的颗粒鸟苷酸环化酶。
DOI: 10.1073/pnas.81.23.7661
发表时间: 1984
影响因子: 11.1
作者:
Winquist,RJ;Faison,EP;Waldman,SA;Schwartz,K;Murad,F;Rapoport,RM
通讯作者: Rapoport,RM
DOI: 10.1073/pnas.79.2.495
发表时间: 1982
影响因子: 11.1
作者:
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DOI: --
发表时间: 1985-03
期刊: The Journal of pharmacology and experimental therapeutics
影响因子: --
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通讯作者: W. Martin;G. Villani;D. Jothianandan;R. Furchgott
DOI: 10.1152/ajpheart.1986.250.5.h822
发表时间: 1986-05-01
影响因子: --
作者:
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DOI: 10.1016/0167-4889(86)90040-6
发表时间: 1986-01
期刊: Biochimica et biophysica acta
影响因子: --
作者:
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通讯作者: Dale C. Leitmans;F. Murad