Barrett J A, DePaul Lynch V, Balkon J, Smith R D, Wolf P S
Pharmacology. 1986;33(3):139-47. doi: 10.1159/000138211.
Anoxia has been shown to potentiate the constrictor effects of 5-hydroxytryptamine (5HT) in isolated vascular tissue. In the present study, canine coronary arterial rings were incubated with various treatments and exposed to 5HT (4 X 10(-7) M) and anoxia (95% N2 and 5% CO2). Developed tension was increased by 250 +/- 40 mg by 5HT alone and 2,000 +/- 90 mg by 5HT and anoxia. Calcium (5 mM) potentiated, while inorganic (lanthanum, 10(-2) M) and organic calcium antagonists (nifedipine, verapamil and diltiazem; IC50 = 7 X 10(-9), 7.3 X 10(-8) and 2.4 X 10(-7) M, respectively) blocked the anoxic potentiation. Anoxia alone decreased resting tension (RT). Methysergide 3 X 10(-5) M inhibited both the 5HT- and anoxia-potentiated responses. Nitroglycerin decreased RT and inhibited the anoxic response (IC50 = 7.6 X 10(-6) M), while dipyridamole decreased RT and did not affect the anoxic response. These data suggest that the potentiation of 5HT contraction by anoxia is dependent upon extracellular calcium influx and is linked to a 5HT receptor. In addition, inhibition of the anoxic response can be achieved at other sites and is not a property common to all coronary vasodilators.
缺氧已被证明可增强5-羟色胺(5HT)对离体血管组织的收缩作用。在本研究中,犬冠状动脉环经不同处理后,暴露于5HT(4×10⁻⁷M)和缺氧环境(95% N₂和5% CO₂)中。单独使用5HT时,收缩张力增加250±40mg,而5HT与缺氧共同作用时,收缩张力增加2000±90mg。钙(5mM)可增强作用,而无机钙拮抗剂(镧,10⁻²M)和有机钙拮抗剂(硝苯地平、维拉帕米和地尔硫䓬;IC₅₀分别为7×10⁻⁹、7.3×10⁻⁸和2.4×10⁻⁷M)可阻断缺氧增强作用。单纯缺氧可降低静息张力(RT)。3×10⁻⁵M的麦角新碱可抑制5HT和缺氧增强的反应。硝酸甘油可降低RT并抑制缺氧反应(IC₅₀ = 7.6×10⁻⁶M),而双嘧达莫可降低RT但不影响缺氧反应。这些数据表明,缺氧对5HT收缩的增强作用依赖于细胞外钙内流,并与5HT受体相关。此外,可在其他部位实现对缺氧反应的抑制,这并非所有冠状动脉扩张剂的共同特性。