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目的：观察肾上腺素能受体亚型β１、α１、α２在去甲肾上腺素（ＮＥ）促进肺动脉平滑肌细胞（ＰＡＳＭＣ）增殖中的作用，并观察钙通道阻滞剂的影响．方法：离体培养新西兰兔ＰＡＳＭＣ，采用四唑盐比色法（ＭＴＴ）和３Ｈ－ＴｄＲ参入实验观察ＰＡＳＭＣ增殖和ＤＮＡ合成量的变化．结果：ＮＥ（１×１０－５～１×１０－４ｍｏｌ／Ｌ）对ＰＡＳＭＣ的增殖和ＤＮＡ的合成有显著的促进作用．β１受体阻断剂Ｐｒｏｐｒａｎｏｌｏｌ使四唑盐比色法（ＭＴＴ）的吸光度（Ａ）和３Ｈ－ＴｄＲ参入率分别下降２５％和２１．８％；α１受体阻断剂ｐｒａｚｏｓｉｎ（１×１０－４ｍｏｌ／Ｌ）使ＭＴＴ的Ａ值和３Ｈ－ＴｄＲ参入率分别下降２９．５％和３５．７％；而α２受体阻断剂ｙｏｈｉｍｂｉｎ（１×１０－３ｍｏｌ／Ｌ）无显著影响．钙通道阻滞剂ｖｅｒａｐａｍｉｌ和ｎｉｆｅｄｉｐｉｎｅ（１×１０－６ｍｏｌ／Ｌ）使ＭＴＴ的Ａ下降３１％和３６％，使３Ｈ－ＴｄＲ参入率下降３６％和４０％．结论：ＮＥ能促进ＰＡＳＭＣ的增殖和ＤＮＡ合成，此效应主要是通过β１和α１受体介导的，可能和α２受体无明显关系．细胞内的Ｃａ２＋增加是ＮＥ促进ＰＡＳＭＣ增殖的重要原因．
Objective: To observe the effects of adrenergic receptor subtypes β1, α1 and α2 on the proliferation of pulmonary artery smooth muscle cells (PASMC) by norepinephrine (NE), and observe the effects of calcium channel blockers. Methods: New Zealand rabbit PASMC was cultured in vitro. The proliferation and DNA synthesis of PASMC were observed by MTT assay and 3H-TdR incorporation assay. Results: NE (1 × 10-5 ~ 1 × 10-4 mol / L) significantly promoted the proliferation and DNA synthesis of PASMC. Propranolol, a β1 receptor antagonist, decreased the absorbance (A) and 3H-TdR incorporation of tetrazolium colorimetric (MTT) by 25% and 21.8%, respectively. The α1 receptor antagonist prazosin (1 × 10- 4mol / L) decreased the A value of MTT and the 3H-TdR incorporation by 29.5% and 35.7%, respectively. However, yohimbin (1 × 10-3mol / L), an α2 receptor blocker, had no significant effect. The calcium channel blockers verapamil and nifedipine (1 × 10-6 mol / L) decreased A of MTT by 31% and 36%, respectively, and decreased the incorporation of 3H-TdR by 36% and 40% respectively. CONCLUSION: NE can promote the proliferation and DNA synthesis of PASMC. The effect is mainly mediated by β1 and α1 receptors, which may not be related to α2 receptor. Intracellular Ca2 + increase is an important reason that NE can promote the proliferation of PASMC.