哇巴因诱导人脐动脉产生的早期和晚期收缩

Early and late contraction induced by ouabain in human umbilical arteries.

作者信息

Sato K, Aoki K

机构信息

Second Department of Internal Medicine, Nagoya City University Medical School, Japan.

出版信息

Br J Pharmacol. 1991 Jun;103(2):1525-9. doi: 10.1111/j.1476-5381.1991.tb09821.x.

DOI:10.1111/j.1476-5381.1991.tb09821.x

PMID:1909202

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1908359/

Abstract

Ouabain (3 x 10(-7)-10(-4) M) evoked a biphasic contraction in human umbilical artery that consisted of an early and a late contraction. The Ca(2+)-antagonists, verapamil (10(-7)-10(-5)) M), diltiazem (10(-7)-(10(-5)) M) and nifedipine (10(-9)-10(-7)) M) inhibited the early but not the late contraction. Caffeine (5 mM) changed neither the magnitude of the peak of the biphasic contraction nor the time needed to reach it. 2. Sodium concentration reduction (140 to 0 mM, replaced by N-methyl-D-glucamine, NMG) produced dose-dependent contraction of the arterial strip in 2.5 mM Ca2+ solution after the first treatment with verapamil (10(-5) M) and caffeine (5 mM), but not in Ca(2+)-free solution. 3. After prior treatment with verapamil and caffeine, the amplitude of the ouabain (10(-4) M)-induced late contraction varied, depending on the concentration of Ca2+ (0-2.5 mM) in the medium. 4. Amiloride (5 x 10(-5) M-5 x 10(-4) M), an inhibitor of the Na(+)-Ca2+ exchange system, produced dose-dependent inhibition of the late contraction induced by ouabain (10(-5) M) after prior treatment with verapamil and caffeine. 5. The time needed to reach the peak tension induced by monensin (5 x 10(-7) M) together with ouabain (10(-6) M) was less than that with ouabain alone, but the magnitude of the peak tension was not changed. 6. These results suggest that the early and late contractions caused by ouabain respectively produce a Ca2+ influx through voltage-sensitive Ca2+ channels and Ca2+ entry through sodium-calcium (Na(+)-Ca2+) exchange.

摘要

哇巴因（3×10⁻⁷ - 10⁻⁴ M）可诱发人脐动脉出现双相收缩，包括早期收缩和晚期收缩。钙拮抗剂维拉帕米（10⁻⁷ - 10⁻⁵ M）、地尔硫䓬（10⁻⁷ - 10⁻⁵ M）和硝苯地平（10⁻⁹ - 10⁻⁷ M）可抑制早期收缩，但不抑制晚期收缩。咖啡因（5 mM）既不改变双相收缩峰值的大小，也不改变达到峰值所需的时间。2. 在先用维拉帕米（10⁻⁵ M）和咖啡因（5 mM）处理后，在2.5 mM Ca²⁺溶液中，钠浓度降低（从140 mM降至0 mM，用N - 甲基 - D - 葡糖胺，NMG替代）可使动脉条产生剂量依赖性收缩，但在无Ca²⁺溶液中则不会。3. 在先用维拉帕米和咖啡因处理后，哇巴因（10⁻⁴ M）诱导的晚期收缩幅度会因培养基中Ca²⁺（0 - 2.5 mM）浓度的不同而变化。4. 钠钙交换系统抑制剂阿米洛利（5×10⁻⁵ M - 5×10⁻⁴ M）在先用维拉帕米和咖啡因处理后，可对哇巴因（10⁻⁵ M）诱导的晚期收缩产生剂量依赖性抑制。5. 莫能菌素（5×10⁻⁷ M）与哇巴因（10⁻⁶ M）共同作用时达到峰值张力所需的时间比单独使用哇巴因时短，但峰值张力的大小没有改变。6. 这些结果表明，哇巴因引起的早期和晚期收缩分别通过电压敏感性Ca²⁺通道使Ca²⁺内流以及通过钠钙（Na⁺ - Ca²⁺）交换使Ca²⁺进入。