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Transmission of impulses in the parasympathetic cardiomotor pathway to the sino-atrial node.

机译:副交感神经运动途径中的冲动传递至窦房结。

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摘要

In mammals and other vertebrates the pacemaker cells of the sino-atrial (SA) node are under powerful inhibitory control of parasympathetic postganglionic cardiomotor neurones. The preganglionic neurones are located in the nucleus ambiguus; some are also located in the dorsal motor nucleus of the vagus although their function in the regulation of pacemaker activity is unknown (Jones, 2001). Activation of these preganglionic cardiomotor neurones leads to activation of cholinergic postganglionic neurones in cardiac ganglia, which in turn results in inhibition of the pacemaker cells in the SA node and subsequently in a decrease of heart rate. It is universally propagated in textbook chapters and elsewhere that the synaptic transmission from parasympathetic preganglionic neurones to postganglionic neurones in the cardiac ganglia occurs with a high safety factor without modulation and that the inhibition of pacemaker cells by activation of cholinergic cardiomotor neurones is mainly generated by the opening of potassium channels via the second-messenger adenylate cyclase/cAMP pathway and by suppression of hyperpolarization-activated Na+/K+-channels. These assumptions need to be corrected in view of experimental data published previously and recently.
机译:在哺乳动物和其他脊椎动物中,窦房(SA)结节的起搏器细胞受到副交感神经节后心脏运动神经元的强大抑制控制。神经节前神经元位于歧核中。尽管它们在调节起搏器活动中的功能尚不清楚,但有些也位于迷走神经的背运动核中(Jones,2001)。这些神经节前心脏运动神经元的激活导致心脏神经节中胆碱能神经节后神经元的激活,这继而导致SA结中的起搏器细胞被抑制,进而导致心率降低。它在教科书章节和其他章节中普遍传播,在心脏神经节中从副交感神经节前神经元到神经节后神经元的突触传递具有很高的安全系数,无需调节,并且通过激活胆碱能心脏运动神经元来抑制起搏器细胞主要是由通过第二信使腺苷酸环化酶/ cAMP途径并通过抑制超极化激活的Na + / K +通道打开钾通道。鉴于先前和最近发布的实验数据,需要纠正这些假设。

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