生长抑素对心脏的抑制作用是由于K+通道的激活吗?

S E Freeman, W M Lau, M Szilagyi
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引用次数: 0

摘要

1. 发现生长抑素(SS)可缩短左、右心房动作电位,降低心房收缩力。动作电位缩短可由钾通道阻断药物他克林和维生素d拮抗。它们在减少SS负性肌力作用方面效果较差。用n -乙基马来酰亚胺对完整心房进行烷基化,可以消除AP缩短作用和SS的负性肌力作用。用百日咳毒素预处理豚鼠可消除SS的负性肌力作用,减少AP缩短。4. 结合研究表明,SS与毒蕈碱和腺苷受体之间几乎没有相互作用。5. 提示心脏SS受体与G蛋白- k +通道-腺苷酸环化酶系统连接,该系统类似于毒蕈碱和腺苷受体系统,但不完全相同。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Is the inhibitory effect of somatostatin on the heart due to K+ channel activation?

1. Somatostatin (SS) was found to shorten the action potential of both left and right atrium, and to reduce the force of contraction of the atrium. Action potential shortening was antagonized by the potassium channel blocking drugs tacrine and apamin. They were less effective in reducing the negative inotropic effect of SS. 2. Alkylation of the intact atrium with N-ethylmaleimide abolished both the AP shortening and the negative inotropic effect of SS. 3. Pretreatment of guinea pigs with pertussis toxin abolished the negative inotropic effect of SS and reduced the AP shortening. 4. Binding studies showed there was virtually no interaction between SS and muscarinic and adenosine receptors. 5. It is suggested that the cardiac SS receptor is linked with G protein-K+ channel-adenylyl cyclase system which is analogous to but not identical with the muscarinic and adenosine receptor systems.

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