C型利钠肽扩张猪冠状动脉的作用及机制的研究

摘要

Objective Investigate the influences of C-natriuretic peptides on langendorff-perfused swine heart coronary. Reveal the underlying vasodilatory ability and mechanism of C-natriuretic peptides. Methods Three different groups named the C-Natriuretic Group ( CNP Group) , the Nitroglycerol Group ( GTN Group) , and the NPR-C Receptor Agonist Group ( cANF4-23 Group) were set up.①Each of above groups was perfused by solution of NE,and then was perfused by GTN、CNP and cANF4-23. The vasodilatory influences of CNP and GTN on swine heart coronary arteries and whether cANF4-23 were involved in this procedure were studied .②cANF4-28 was given first, and then CNP were added, the vasodilatory influences were observed.③K + solutions ( at the concentration of 80 nM) were used to preserve the arteries, so they were all in contracted state, and then CNP and cANF4-23 were added, and the vasodilatory influences were observed. Results ①CNP,GTN and cANF4-23 all had significant vasodilatory in-fluences on swine heart coronary artery. no significant difference of vasodilation influences was found between CNP Group and cANF4-23 Group(P>0. 05). The vasodilatory influence of CNP Group was weaker than GTN Group (P<0. 05).②In cANF4-28 preserved arteries, The largest circulus vasculosus vasodilatory ratios of CNP was significantly weaker than Control Group , and had statistical significance (P<0. 01).③The vasodilatory influences of CNP and cANF4-23 Groups were significantly decreased in high concentration K + solution in contrast with the Control Group ( P<0. 05 ) , but not blocked. Conclusions C- Natriuretic peptides have significant vasodilatory influence on swine heart coronary artery. The vasodilatory mechanism of CNP involves NPR-C. NPR-C is not only the well-known clearance receptor, but also leads to vasodilation of the coronary artery. the vasodilatory of CNP/NPR-C sig-naling involves K+ channel.%目的：本研究通过离体灌流方法观察C型利钠肽( CNP)对离体猪冠状动脉血管张力的影响,探讨C型利钠肽的扩血管能力及其机制。方法本实验分为三组：C型利钠肽组( CNP组)、硝酸甘油组( GTN组)、利钠肽受体C (NPR-C)激动剂组(cANF4-23组)。①上述各组中分别加入去甲肾上腺素(NE),然后分别加入GTN、CNP和cANF4-23,比较CNP和硝酸甘油对冠状动脉的扩张能力,并了解cANF4-23是否有扩血管作用。②在CNP组预先加入NPR-C受体抑制剂(cANF4-28),比较加药前后的扩血管作用变化。③80mM高钾溶液预收缩血管,然后分别加入CNP、cANF4-23,观察高钾对CNP和cANF4-23扩血管作用的影响。结果①CNP、NPR-C受体激动剂(cANF4-23)及硝酸甘油均有明显的舒血管作用。 CNP组舒血管作用与cANF4-23组类似,低于GTN组,差异有统计学意义( P<0．05)。②预先加入NPR-C受体抑制剂(cANF4-28),CNP组最大舒张率明显下降,差异有统计学意义(P<0．01)。③高钾溶液中加入CNP、cANF4-23,血管舒张作用明显抑制,与对照组相比差异有统计学意义(P<0．05),但血管舒张作用未被完全抑制。结论本研究阐明CNP对冠状动脉具有良好的舒张作用；CNP主要通过NPR-C受体介导发挥舒血管效应；CNP/NPR-C路径所致的血管舒张主要与钾通道有关。