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上皮完整或去上皮的豚鼠离体气管以３００μｍｏｌ·Ｌ－１硝普钠（ＳＮＰ）预处理１ｈ，使ＳＮＰ对抗乙醋甲胆碱气管收缩作用的剂量反应曲线右移１．３－１．５倍，最大舒张率下降４１％－５８％，形成ＳＮＰ气管松弛作用的耐受性．８－溴环鸟苷酸可模拟ＳＮＰ在豚鼠离体气管形成的ＳＮＰ耐受性，谷胱甘肽（１ｍｍｏｌ·Ｌ－１）及环核苷酸磷酸二酯酶（ＰＤＥ）Ⅴ抑制剂扎普司特（３０μｍｏｌ·Ｌ－１）均可部分翻转ＳＮＰ的气管松弛作用耐受性，而蛋白合成抑制剂环己酰亚胺（１０μｍｏｌ·Ｌ－１）对ＳＮＰ的耐受性无预防作用．结果表明ＳＮＰ可产生豚鼠离体气管松弛耐受性，这可能是由于气管平滑肌中环鸟苷酸（ｃＧＭＰ）积聚而下调鸟苷酸环化酶（ＧＣ）活性和上调ＰＤＥⅤ活性．
The guinea pigs with epithelial integrity or decellularization were pretreated with 300 μmol·L-1 sodium nitroprusside (SNP) for 1 h, and the dose response curve of SNP against trachoma of ethyl methacholine shifted to the right by 1.3-1.5 Times, the maximum relaxation rate decreased by 41% -58%, the formation of SNP tracheal relaxation tolerance. 8-Bromoguanosine mimics the SNP tolerance of SNP in guinea pig tracheal formation, glutathione (1 mmol·L-1) and cyclic nucleotide phosphodiesterase (PDE) Ⅴ inhibitor Zap Stevioside (30μmol·L-1) partially reversed the tracheal relaxation tolerance of SNP, while cycloheximide (10μmol·L-1) had no preventive effect on SNP tolerance. The results show that SNP can induce tracheal relaxation tolerance in isolated guinea pigs, which may be due to the accumulation of cyclic guanylate (cGMP) in the tracheal smooth muscle, down-regulating guanylate cyclase (GC) activity and up-regulating PDE V activity.