ENDOTHELIAL-CELLS AS MEDIATORS OF VASODILATION OF ARTERIES
ENDOTHELIAL-CELLS AS MEDIATORS OF VASODILATION OF ARTERIES
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DOI：
10.1097/00005344-198406002-00008
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发表时间：
1984-01-01
影响因子：
3
通讯作者：
JOTHIANANDAN, D
中科院分区：
文献类型：
--
作者：
FURCHGOTT, RF;CHERRY, PD;JOTHIANANDAN, D
首先简要回顾了作者和其他人在过去几年中对大量血管活性药物对离体动脉的非前列腺素内皮依赖性舒张作用的研究结果。这些药物包括乙酰胆碱（ACh）;钙离子载体A23187; ATP和ADP; P物质;缓激肽（犬、人和猪动脉）;组胺，通过H1受体起作用（大鼠动脉）;凝血酶（犬动脉）;血清素（犬冠状动脉）;和去甲肾上腺素，通过α 2受体起作用（犬冠状动脉）。ACh和其他药物释放的内皮源性舒张因子（EDRF）尚未确定。我们最初的假设，花生四烯酸是前体的EDRF是不支持的发现，其他不饱和脂肪酸除了花生四烯酸，甚至硬脂酸，引起非前列腺素内皮依赖性舒张。亚甲蓝和血红蛋白（而不是高铁血红蛋白）迅速抑制ACh或A23187舒张兔主动脉，这表明我们的建议，EDRF是一个不稳定的自由基可能是正确的。内皮依赖性舒张由这些代理商被证明是由内皮依赖性增加环GMP在平滑肌中的一个发现一致的假设，即EDRF刺激鸟苷酸环化酶在肌肉中，导致增加环GMP，以某种方式激活放松。一些问题有关的内皮依赖性舒张的潜在生理重要性进行了讨论。
A brief review is first presented of findings during the past few years by the authors and by others on the nonprostaglandin endothelium-dependent relaxation of isolated arteries by a large number of vasoactive agents. Among these agents are acetylcholine (ACh); the calcium ionophore A23187; ATP and ADP; substance P; bradykinin (canine, human, and porcine arteries); histamine, acting via an H1-receptor (rat arteries); thrombin (canine arteries); serotonin (canine coronary artery); and norepinephrine, acting via an [alpha] 2-receptor (canine coronary artery). The endothelium-derived relaxing factor (EDRF) released by ACh and other agents has not yet been identified. Our original hypothesis that arachidonic acid is the precursor of EDRF is not supported by the finding that other unsaturated fatty acids in addition to arachidonic acid, and even stearic acid, elicited nonprostaglandin endothelium-dependent relaxations. Methylene blue and hemoglobin (but not methemoglobin) rapidly inhibited relaxation of rabbit aorta by ACh or A23187, suggesting that our proposal that EDRF is a labile free radical may be correct. The endothelium-dependent relaxation by each of these agents was shown to be preceded by an endothelium-dependent increase in cyclic GMP in the smooth muscle-a finding consistent with the hypothesis that EDRF stimulates guanylate cyclase in the muscle, leading to an increase in cyclic GMP that somehow activates relaxation. Some questions relating to the potential physiological importance of endothelium-dependent relaxations are discussed.