Sabouni M H, Mustafa S J
Department of Pharmacology, School of Medicine, East Carolina University, Greenville, NC 27834.
Eur J Pharmacol. 1989 Sep 22;168(3):271-6. doi: 10.1016/0014-2999(89)90787-5.
The effects of adenosine receptor agonists and ouabain on rhythmicity were studied in coronary arteries obtained from 12 human donors. Ring segments of left anterior descending coronary arteries were suspended in organ baths for measurement of isometric tension. Prostaglandin F2 alpha (PGF2 alpha:10 microM) produced tonic contractions followed by phasic relaxations. The phasic relaxations were completely abolished by either 100 nM ouabain or 50 mM KCl and changed to tonic contraction. The rhythmicity was also inhibited in K+-free medium. The adenosine analogs, 5'-N-ethylcarbo-xamidoadenosine (NECA) and 2-chloroadenosine (CAD) caused a concentration-dependent relaxation of the maximum force, minimum force, and decreased the frequency of rhythmicity. In rings that did not show phasic activity in response to PGF2 alpha, NECA and CAD produced concentration-dependent relaxation of the tonic contraction. Prior treatment with ouabain (100 nM) prevented the relaxing response of these compounds and the development of rhythmicity. Our data show that PGF2 alpha-induced rhythmicity in human coronary arteries could be inhibited by ouabain, alterations in K+ concentrations and by adenosine analogs. The relaxations produced by adenosine analogs could also be inhibited by ouabain.
在取自12位人类供体的冠状动脉中研究了腺苷受体激动剂和哇巴因对节律性的影响。将左前降支冠状动脉的环段悬挂于器官浴槽中以测量等长张力。前列腺素F2α（PGF2α：10微摩尔）引起强直性收缩，随后是阶段性舒张。100纳摩尔哇巴因或50毫摩尔氯化钾均可完全消除阶段性舒张，并使其转变为强直性收缩。在无钾培养基中节律性也受到抑制。腺苷类似物5'-N-乙基甲酰胺基腺苷（NECA）和2-氯腺苷（CAD）引起最大力、最小力的浓度依赖性舒张，并降低节律频率。在对PGF2α无阶段性活动表现的环段中，NECA和CAD引起强直性收缩的浓度依赖性舒张。预先用哇巴因（100纳摩尔）处理可阻止这些化合物的舒张反应以及节律性的产生。我们的数据表明，哇巴因、钾离子浓度改变以及腺苷类似物均可抑制PGF2α诱导的人冠状动脉节律性。腺苷类似物产生的舒张也可被哇巴因抑制。
