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观察血管钠肽（VNP）对慢性缺氧大鼠离休肺动脉、腹主动脉和腹腔静脉的舒张作用及内皮细胞的存在与否、ATP敏感性钾通道（K(ATP)）和β受体阻断剂对其作用的影响．方法：采用离体血管灌流方法，以去甲肾上腺素（NE，10μmol／L）使血管环收缩的效应为基础，测定VNP对血管环张力的影响，求出最大舒张反应值（E(max)）．结果：VNP对慢性缺氧大鼠的保留或去内皮的肺动脉、腹主动脉和腹腔静脉均有浓度依赖性舒张作用．内皮完整的肺动脉、腹主动脉和腹腔静脉对VNP的E(max)分别为（83±7）％，（60±5）％和（62±7）％．VNP对肺动脉的舒张作用明显强于腹主动脉和腹腔静脉（P＜0．05），但在保留内皮组与去内皮组间无显著差异（P＞0．05）．在浴槽内预先孵育优降糖（1μmol／L）或心得安（3μmol／L）可显著降低上述3种血管对VNP的舒张效应．结论：新合成的VNP是一个强效的和非内皮依赖性的血管松弛多肽，其舒血管作用部分受K(ATP)通道和β受体阻断剂的调控．
To observe the vasodilatory effect of vascular sodium peptide (VNP) on pulmonary artery, abdominal aorta and celiac vein in rats with chronic hypoxia, the existence of endothelial cells, ATP-sensitive potassium channel (K (ATP) The effect of agents on their effects. Methods: The effects of VNP on the tension of vascular rings were determined based on the effect of norepinephrine (NE, 10μmol / L) on the contraction of the vascular rings. The maximum diastolic response (E (max) ). RESULTS: VNP had a concentration-dependent relaxation effect on the retained or endothelium-derived pulmonary artery, abdominal aorta and celiac vein in rats with chronic hypoxia. E (max) of VNP for intact endothelium of pulmonary artery, abdominal aorta and celiac vein were (83 ± 7)%, (60 ± 5)% and (62 ± 7)%, respectively. The vasodilatation effect of VNP on the pulmonary artery was significantly stronger than that of the abdominal aorta and the celiac vein (P <0.05), but no significant difference was found between the preserved endothelium and the endothelium (P> 0.05). Pre-incubation of glibenclamide (1 μmol / L) or propranolol (3 μmol / L) in the bath significantly reduced the vasorelaxation effect of VNP on the above three vessels. Conclusion: The newly synthesized VNP is a potent and non-endothelium-dependent vascular relaxant peptide whose vasodilatory activity is regulated in part by K (ATP) channels and β-blockers.