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血管活性物质在完整豚鼠心内膜内皮细胞中诱导的超极化

Hyperpolarization induced by vasoactive substances in intact guinea-pig endocardial endothelial cells.

作者信息

Manabe K, Ito H, Matsuda H, Noma A

机构信息

Department of Physiology, Faculty of Medicine, Kyushu University, Fukuoka, Japan.

出版信息

J Physiol. 1995 Apr 1;484 ( Pt 1)(Pt 1):25-40. doi: 10.1113/jphysiol.1995.sp020645.

Abstract
  1. The responses of guinea-pig endocardial endothelial (EE) cells to various vasoactive substances were investigated in either the small tissue preparation or freshly isolated cells using the patch clamp technique. 2. The mean resting potential of the EE cell was -44 mV in the small tissue preparation, and applications of ATP, ADP, AMP, adenosine, histamine and substance P induced transient hyperpolarizations of -22, -21, -9, -10, -23 and -15 mV, respectively. The membrane potential of EE cells failed to respond to acetylcholine, bradykinin, thrombin, atrial natriuretic peptide, vasopressin and serotonin. 3. The whole-cell voltage clamp of dissociated cells revealed a transient increase of K+ conductance underlying the ATP and histamine responses. The agonist-induced current showed no time-dependent change during voltage steps. The response was showed no time-dependent change during voltage steps. The response was prevented by adding 10 mM EGTA to the pipette solution. 4. In the cell-attached single channel recordings, ATP induced transient K+ channel activities having a slope conductance of 34 pS. In inside-out patches, similar K+ channels were activated by applying Ca2+ of more than 0.1 microM. 5. These findings are consistent with the idea that the Ca(2+)-dependent K+ channel is involved in the hyperpolarizing response of EE cells, as described in vascular endothelial cells.
摘要
  1. 采用膜片钳技术,在小型组织标本或新鲜分离的细胞中研究了豚鼠心内膜内皮(EE)细胞对各种血管活性物质的反应。2. 在小型组织标本中,EE细胞的平均静息电位为-44 mV,应用ATP、ADP、AMP、腺苷、组胺和P物质分别诱导了-22、-21、-9、-10、-23和-15 mV的瞬时超极化。EE细胞的膜电位对乙酰胆碱、缓激肽、凝血酶、心房利钠肽、血管加压素和5-羟色胺无反应。3. 对解离细胞进行全细胞膜片钳记录显示,ATP和组胺反应的基础是K+电导的瞬时增加。激动剂诱导的电流在电压钳制步骤中未显示出时间依赖性变化。该反应在电压钳制步骤中也未显示出时间依赖性变化。通过向微电极溶液中加入10 mM EGTA可阻止该反应。4. 在细胞贴附式单通道记录中,ATP诱导了斜率电导为34 pS的瞬时K+通道活性。在向外膜片记录中,施加浓度大于0.1 microM的Ca2+可激活类似的K+通道。5. 这些发现与以下观点一致,即如血管内皮细胞中所述,Ca(2+)依赖性K+通道参与了EE细胞的超极化反应。

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