Gajewski M, Laskowska-Bozek H, Moutiris J A, Maśliński S, Ryzewski J
Department of Biochemistry, Institute of Rheumatology, Warsaw, Poland.
Acta Neurobiol Exp (Wars). 1993;53(1):79-91.
In contrast to adrenaline, exogenously administered cholinergic agonist, carbachol have very little effect on the contractility of rat cardiac myocytes, unless its contractile has been increased by adrenergic agonist. This interaction between the muscarinic and adrenergic pathways has been suggested to be the major means by which muscarinic agonist alters adrenergic function. When the cardiac myocytes were incubated in the medium contained the mitochondrial respiratory inhibitor potassium cyanide (chemically-induced hypoxia) the spontaneous contractility was ceased. The contractility partly recovered when the cells were exposed to adrenergicstimulation. We showed that during chemical hypoxia, in which cellular ATP is decreased (37% of control), the responsiveness of myocytes to muscarinic cholinergic stimulation significantly increase. Contraction of myocytes, stimulated by adrenaline was totally inhibited by 10(-4)M of carbachol in control cells and 5 x 10(-6)M of carbachol in cells with chemically-induced hypoxia. This increase in physiological response to muscarinic stimulation was associated with an increase of muscarinic receptors (630%). The results support the hypothesis that in ischaemic/hypoxic myocardium the role of cholinergic system may be more important than previously assumed.
与肾上腺素不同，外源性给予的胆碱能激动剂卡巴胆碱对大鼠心肌细胞的收缩性影响很小，除非其收缩性已被肾上腺素能激动剂增强。毒蕈碱和肾上腺素能途径之间的这种相互作用被认为是毒蕈碱激动剂改变肾上腺素能功能的主要方式。当心肌细胞在含有线粒体呼吸抑制剂氰化钾的培养基中孵育（化学诱导的缺氧）时，自发收缩性停止。当细胞受到肾上腺素能刺激时，收缩性部分恢复。我们表明，在化学缺氧期间，细胞内ATP减少（对照组的37%），心肌细胞对毒蕈碱胆碱能刺激的反应性显著增加。在对照细胞中，10(-4)M的卡巴胆碱和在化学诱导缺氧的细胞中5×10(-6)M的卡巴胆碱可完全抑制肾上腺素刺激的心肌细胞收缩。对毒蕈碱刺激的生理反应增加与毒蕈碱受体增加（630%）有关。结果支持了这样的假设，即在缺血/缺氧心肌中，胆碱能系统的作用可能比以前认为的更重要。
