Ledda F, Corti V, Mantelli L
Department of Pharmacology, University of Florence, Italy.
Eur J Pharmacol. 1989 Mar 21;162(2):323-7. doi: 10.1016/0014-2999(89)90295-1.
The cardiac response to adrenergic nerve stimulation was dose dependently reduced in a statistically significant manner by 1-10 microM dynorphin-(1-13) in isolated atria, and by 0.1-1 microM dynorphin-(1-13) in guinea-pig ventricular preparations. The inhibitory effect of dynorphin was maintained in atria that had been pretreated with two cyclooxygenase inhibitors at concentrations that induce an 80% inhibition of the enzyme, namely indomethacin 3 microM and acetylsalicylic acid 200 microM. The inhibitory effect of dynorphin disappeared in similarly pretreated ventricular preparations. These results suggest that, whilst the mediation of the effect of dynorphin is carried out mainly by specific opioid receptors in the atrial section, in the ventricular tissue it occurs through the endogenous prostanoid system.
在离体心房中，1 - 10微摩尔强啡肽 -（1 - 13）可使心脏对肾上腺素能神经刺激的反应呈剂量依赖性降低，且具有统计学意义；在豚鼠心室标本中，0.1 - 1微摩尔强啡肽 -（1 - 13）也有此作用。强啡肽的抑制作用在预先用两种环氧化酶抑制剂处理过的心房中依然存在，这两种抑制剂的浓度能使该酶的活性受到80%的抑制，即3微摩尔的吲哚美辛和200微摩尔的乙酰水杨酸。而在同样预先处理过的心室标本中，强啡肽的抑制作用消失了。这些结果表明，虽然强啡肽作用的介导主要通过心房部分的特异性阿片受体进行，但在心室组织中，其作用是通过内源性前列腺素系统发生的。
