C型利钠肽舒张兔主动脉作用机制的探讨

Vasodilatory Effects of CNP on Aortic Arteries of Rabbits

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 mechanism of vasodilatory effects of C-type natriuretic peptide(CNP).Methods Tension changes in aortic rings of rabbits were recorded with the presence of CNP or C-type natriuretic peptide receptor(NPR-C) agonist(cANF4-23) after pretreatment with epinephrine(NE) or 60 mmol/L KCl.The vasodilatory effects of four types of potassium channel blocker and NPR-C antagonist(cANF4-28) were also tested.Results A maximal vasorelaxant effects of(33.5±5.9)% and(38.4±10.6)% were recorded in the presence of 1 μmol/L CNP and cANF4-23,respectively.cANF4-28 attenuated the action of CNP((19.8±8.3)%).The vasorelaxant effects of CNP and cANF4-23 decreased significantly after pretreatment with 60 mmol/L KCl(P<0.01).Glibenclamide and BaCl2 also attenuated the relaxant activities of CNP(P<0.05).But only BaCl2 decreased the vasodilatory action of cANF4-23(P<0.05).Conclusion The relaxant activity of CNP is mediated through three paths: NPR-B/KATP,NPR-C/KIR and NPR-C/calcium channels.