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目的探讨C型利钠肽(CNP)舒张血管的受体和通道机制。方法采用兔胸主动脉环张力测定法,观察CNP和C型利钠肽受体(NPR-C)激动剂cANF4-23对肾上腺素(NE)10μmol/L或氯化钾(KCl)60 mmol/L预收缩血管的舒张作用,及多种钾通道阻断剂对两者舒血管效应的影响。结果 1μmol/L CNP和cANF4-23对血管的最大舒张率分别为(33.5±5.9)%、(38.4±10.6)%,两组舒血管作用比较差异无统计学意义(P>0.05);NPR-C受体阻断剂能减弱CNP的舒血管作用〔(19.8±8.3)%〕;高钾预收缩后CNP、cANF4-23对血管舒张作用明显降低(P<0.01);优降糖或氯化钡能明显抑制CNP的血管舒张作用(P<0.05);氯化钡使cANF4-23的血管舒张作用明显降低(P<0.05)。结论 NPR-C/内向整流钾通道(KIR)、NPR-C/钙通道和B型利钠肽受体(NPR-B)/ATP敏感钾通道(K)参与了CNP对兔主动脉的舒张作用。
Objective To investigate the receptor and channel mechanism of C-type natriuretic peptide (CNP) relaxing blood vessels. Methods Tension measurement of thoracic aorta rings was used to observe the effect of cANF4-23, a CNP and C-type natriuretic peptide receptor (NPR-C) agonist, on 10 μmol / L epinephrine (NE), 60 mmol / L pre-contractile vasodilatation, and a variety of potassium channel blockers on both vasodilator effect. Results The maximal relaxation rate of 1 μmol / L CNP and cANF4-23 was (33.5 ± 5.9)% and (38.4 ± 10.6)%, respectively. There was no significant difference in the vasodilatation between the two groups (P> 0.05) (19.8 ± 8.3)%]; CNP and cANF4-23 significantly reduced the vasodilatation (P <0.01) after precontraction of high potassium (P <0.01) Barium can significantly inhibit the vasodilation of CNP (P <0.05); barium chloride reduced the vasodilation of cANF4-23 significantly (P <0.05). CONCLUSIONS: NPR-C / KIR, NPR-C / calcium channel and NPR-B / ATP-sensitive potassium channel (K) are involved in the relaxation of CNP in rabbit aorta .