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促肠动素可诱导鲎心肌产生节律性收缩和尖峰电位。

Proctolin induces rhythmic contractions and spikes in Limulus heart muscle.

作者信息

Watson W H, Hoshi T

出版信息

Am J Physiol. 1985 Oct;249(4 Pt 2):R490-5. doi: 10.1152/ajpregu.1985.249.4.R490.

Abstract

The Limulus heart is neurogenic. If the cardiac ganglion is removed, all spontaneous contractions of the heart are abolished. Application of the pentapeptide proctolin (greater than 1 microM) causes the deganglionated heart muscle to beat with a frequency and amplitude slightly greater than those of a normal heart with an intact cardiac ganglion. At a proctolin concentration of 1 microM, rhythmic beating requires 2-10 min to develop, and up to 1 h of continuous washing is required to reverse the effect. A contracture often precedes the rhythmic contractions. Proctolin-induced rhythmicity occurs in the presence of tetrodotoxin (TTX) and in Na+-free saline. These effects of proctolin are not mediated by residual portions of the cardiac ganglion. Contractions are inhibited by Ca2+-free EGTA saline, CoCl2, MnCl2, and CdCl2. Proctolin causes no significant long-term changes in the myocardial resting potential or apparent input resistance. However, proctolin causes rhythmic 10- to 20-mV spikes that precede each contraction of the myocardium. Production of these spikes appears to be the mechanism by which proctolin causes rhythmic contractions in normally quiescent deganglionated myocardium of Limulus.

摘要

鲎的心脏是神经源性的。如果切除心脏神经节,心脏的所有自发收缩都会消失。应用五肽促肠肌肽(大于1微摩尔)会使去神经节的心肌以略高于具有完整心脏神经节的正常心脏的频率和幅度跳动。在促肠肌肽浓度为1微摩尔时,有节律的跳动需要2至10分钟才能形成,并且需要长达1小时的连续冲洗才能逆转这种作用。挛缩通常先于节律性收缩出现。促肠肌肽诱导的节律性在河豚毒素(TTX)存在和无钠盐溶液中都会发生。促肠肌肽的这些作用不是由心脏神经节的残留部分介导的。收缩受到无钙EGTA盐溶液、氯化钴、氯化锰和氯化镉的抑制。促肠肌肽不会引起心肌静息电位或表观输入电阻的显著长期变化。然而,促肠肌肽会在心肌每次收缩之前引起10至20毫伏的节律性尖峰。这些尖峰的产生似乎是促肠肌肽在正常静止的去神经节鲎心肌中引起节律性收缩的机制。

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