HETEROGENEOUS DISTRIBUTION OF ENDOTHELIUM-DEPENDENT RELAXATIONS RESISTANT TO NG-NITRO-L-ARGININE IN RATS
HETEROGENEOUS DISTRIBUTION OF ENDOTHELIUM-DEPENDENT RELAXATIONS RESISTANT TO NG-NITRO-L-ARGININE IN RATS
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DOI：
10.1152/ajpheart.1992.263.4.h1090
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发表时间：
1992-10-01
影响因子：
--
通讯作者：
VANHOUTTE, PM
中科院分区：
文献类型：
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作者：
NAGAO, T;ILLIANO, S;VANHOUTTE, PM
对一氧化氮合酶抑制剂有抵抗力的内皮依赖性舒张可能是由血管平滑肌的内皮依赖性超极化介导的。通过测量等长力的变化，进行实验以检查这种类型的松弛沿着大鼠动脉树的分布。乙酰胆碱诱导的浓度和内皮依赖性舒张在动脉和肺动脉，髂总动脉，股动脉，肠系膜和肾动脉与苯乙醯胺收缩。在存在N（G）-硝基-L-精氨酸的情况下，乙酰胆碱的累积给药仅在股动脉、肠系膜动脉和肾动脉中引起舒张。钙离子载体A23187以浓度依赖性和内皮依赖性方式舒张苯肾上腺素收缩的肠系膜动脉。在N（G）-硝基-L-精氨酸存在下，A23187的浓度-松弛曲线右移。钾离子通道开放剂lemakalim诱导的最大舒张作用在未表现出N（G）-硝基-L-精氨酸抵抗性舒张作用的动脉中较小。这些结果表明，N（G）-硝基-L-精氨酸抵抗性舒张在较小的动脉中更常见。表现出N（G）-硝基-L-精氨酸抗性舒张的动脉可能对引起血管平滑肌细胞超极化的内皮源性物质更敏感。
Endothelium-dependent relaxations that are resistant to inhibitors of nitric oxide synthase probably are mediated by endothelium-dependent hyperpolarization of the vascular smooth muscle. Experiments were performed to examine the distribution of this type of relaxation along the arterial tree of the rat by measuring changes in isometric force. Acetylcholine induced concentration- and endothelium-dependent relaxations in aortas and in pulmonary, common iliac, femoral, mesenteric, and renal arteries contracted with phenylephrine. In the presence of N(G)-nitro-L-arginine, the cumulative administration of acetylcholine induced relaxations only in the femoral, mesenteric, and renal arteries. The calcium ionophore A23187 relaxed mesenteric arteries contracted with phenylephrine in a concentration-and endothelium-dependent manner. The concentration-relaxation curve to A23187 was shifted to the right in the presence of N(G)-nitro-L-arginine. The maximal relaxations induced by lemakalim, a K+ channel opener, were smaller in those arteries that did not exhibit N(G)-nitro-L-arginine-resistant relaxations. These results suggest that N(G)-nitro-L-arginine-resistant relaxations are more frequently observed in smaller arteries. The arteries that exhibit N(G)-nitro-L-arginine-resistant relaxations may be more sensitive to an endothelium-derived substance that causes hyperpolarization of vascular smooth muscle cells.