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ATP敏感性钾通道与冠状动脉基础血管张力

KATP channels and basal coronary vascular tone.

作者信息

Daut J, Klieber H G, Cyrys S, Noack T

机构信息

Physiologisches Institut, Technischen Universität München, Germany.

出版信息

Cardiovasc Res. 1994 Jun;28(6):811-7. doi: 10.1093/cvr/28.6.811.

DOI:10.1093/cvr/28.6.811
PMID:7923284
Abstract

After reviewing recent experimental work from various laboratories we have come to the following conclusions. (1) An increase in transmural pressure causes depolarisation of coronary arterioles, which increases smooth muscle tone. Under these conditions the opening of KATP channels can induce a much larger change in membrane potential than in relaxed arteries. Furthermore, the rate of ATP hydrolysis by contractile proteins, and thus the submembrane nucleotide concentrations, might also be changed in the presence of myogenic tone. Therefore care should be taken when extrapolating patch clamp results from isolated coronary smooth muscle cells to the function of KATP channels in vivo. (2) The opening of KATP channels is increased in situations related to energy imbalance, such as hypoxia, adenosine release, intracellular acidification, and lactate accumulation. However, there is increasing evidence that KATP channels also contribute to the setting of the membrane potentials of coronary smooth muscle cells under normoxic conditions. Thus the modulation of KATP channels by intracellular metabolites and by vasoactive autacoids may play an important role in the regulation of coronary blood flow even in the presence of normal intracellular ATP concentrations. (3) The smooth muscle cells of coronary terminal arterioles form an electrical syncytium. The opening of a new KATP channels in smooth muscle cells of a terminal arterioles might induce a spatially homogeneous hyperpolarisation of the entire arteriole. The resulting homogeneous decrease in the tone of the coronary smooth muscle cells of the arteriole may induce a considerable change in vascular resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

在回顾了各实验室近期的实验工作后,我们得出了以下结论。(1)跨壁压力增加会导致冠状动脉小动脉去极化,从而增加平滑肌张力。在这些情况下,ATP敏感性钾通道(KATP通道)的开放所诱导的膜电位变化可能比舒张状态的动脉大得多。此外,收缩蛋白水解ATP的速率,进而细胞膜下核苷酸浓度,在存在肌源性张力的情况下也可能发生变化。因此,将膜片钳实验结果从分离的冠状动脉平滑肌细胞外推至体内KATP通道的功能时应谨慎。(2)在与能量失衡相关的情况下,如缺氧、腺苷释放、细胞内酸化和乳酸堆积,KATP通道的开放会增加。然而,越来越多的证据表明,在常氧条件下KATP通道也参与冠状动脉平滑肌细胞膜电位的设定。因此,即使在细胞内ATP浓度正常的情况下,细胞内代谢产物和血管活性自分泌物质对KATP通道的调节可能在冠状动脉血流调节中起重要作用。(3)冠状动脉终末小动脉的平滑肌细胞形成电突触。终末小动脉平滑肌细胞中新的KATP通道开放可能会诱导整个小动脉在空间上均匀的超极化。由此导致的小动脉冠状动脉平滑肌细胞张力均匀降低可能会引起血管阻力的显著变化。(摘要截取自250词)

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