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为了研究血管钠肽 (VNP)对人乳内动脉 (humanintramammaryartery ,HIMA)的舒张作用及其机制 ,采用离体血管灌流的方法 ,观察VNP对内皮完整和去内皮HIMA的舒张作用 ,以及HS 142 1、TEA、8 Br cGMP和镁蓝 (MB)对这一过程的影响。实验中观察到 ,VNP ( 0 0 0 0 1- 1μmol/L)可引起剂量依赖性的舒张效应 ,且无内皮依赖性 ;8 Br cGMP ( 0 1- 10 0 0 μmol/L)也可引起剂量依赖性的血管舒张效应。钠尿肽鸟苷酸环化酶 (guanylatecy clase ,GC)受体的特异性阻断剂HS 142 1( 2 0 μmol/L)使VNP舒张HIMA的作用几乎完全消失。MB是GC的抑制剂 ,10 μmol/L的MB不但使VNP舒张HIMA的作用完全消失 ,而且可增强HIMA对去甲肾上腺素 (NE)产生的收缩反应。钙激活钾通道 (KCa)的阻断剂TEA( 1mmol/L)可减弱 (但是不完全阻断 )VNP的舒血管作用。上述结果表明 ,VNP对HIMA具有不依赖内皮的舒张作用 ;此作用是通过作用于平滑肌细胞的钠尿肽GC受体 ,引起细胞内的cGMP水平升高实现的 ,并且与KCa有关
In order to investigate the vasodilation effect and mechanism of VNP on human intratumoral arterial arteries (HIMA), the vasodilatory effect of VNP on intact endothelial and endothelium-derived HIMA was observed by means of ex vivo vascular perfusion. HS 142 1 , TEA, 8 Br cGMP and Magnesium Blue (MB) on this process. In the experiment, it was observed that VNP (0 0 0 0 1 - 1μmol / L) induced a dose-dependent relaxation effect and no endothelium-dependent effect; 8 Br cGMP (0 1 -10 0 0 μmol / L) Dependent vasodilatory effects. The specific blocker HS 142 1 (20 μmol / L) of natriuretic peptide guanylatecysecrase (GC) receptor almost completely abolished the vasodilation of HIMA by VNP. MB is an inhibitor of GC. MB at 10 μmol / L not only completely abolished the effect of vasodilatation of HIMA on VNP, but also enhanced the contractile response of norepinephrine (NE) to HIMA. TEA (1 mmol / L), a blocker of calcium-activated potassium channels (KCa), attenuated (but did not completely block) the vasorelaxing effect of VNP. The above results indicate that VNP has an endothelial-independent relaxation effect on HIMA by acting on the natriuretic peptide GC receptor of smooth muscle cells, resulting in an increase of intracellular cGMP levels and is associated with KCa