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本文引用的文献

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An estimate of the calcium content of the sarcoplasmic reticulum in rat ventricular myocytes.大鼠心室肌细胞肌浆网钙含量的估计
Pflugers Arch. 1993 Apr;423(1-2):158-60. doi: 10.1007/BF00374975.
2
The role of sarcoplasmic reticulum and Na-Ca exchange in the Ca2+ extrusion from the resting myocytes of guinea-pig heart: comparison with rat.肌浆网和钠钙交换在豚鼠心脏静息心肌细胞钙外流中的作用:与大鼠的比较。
J Mol Cell Cardiol. 1993 Jan;25(1):75-91. doi: 10.1006/jmcc.1993.1009.
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Cell signalling. A tale of two messengers.细胞信号传导。两个信使的故事。
Nature. 1993 Sep 30;365(6445):388-9. doi: 10.1038/365388a0.
4
Involvement of stretch-activated ion channels in Ca2+ mobilization to mechanical stretch in endothelial cells.牵张激活离子通道在内皮细胞中钙离子动员对机械牵张的参与。
Am J Physiol. 1993 Apr;264(4 Pt 1):C1037-44. doi: 10.1152/ajpcell.1993.264.4.C1037.
5
Mechanical stretch rapidly activates multiple signal transduction pathways in cardiac myocytes: potential involvement of an autocrine/paracrine mechanism.机械牵张可迅速激活心肌细胞中的多种信号转导通路:自分泌/旁分泌机制的潜在参与。
EMBO J. 1993 Apr;12(4):1681-92. doi: 10.1002/j.1460-2075.1993.tb05813.x.
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Extracellular fluid translocation in perfused rabbit atria: implication in control of atrial natriuretic peptide secretion.灌注兔心房中的细胞外液转运:对心房利钠肽分泌控制的影响
J Physiol. 1993 Aug;468:591-607. doi: 10.1113/jphysiol.1993.sp019790.
7
Effect of ryanodine on atrial natriuretic peptide secretion by contracting and quiescent rat atrium.兰尼碱对收缩和静止大鼠心房利钠肽分泌的影响。
Pflugers Arch. 1994 Feb;426(3-4):276-83. doi: 10.1007/BF00374782.
8
Stretch-activated ion channels in tissue-cultured chick heart.组织培养的鸡心脏中的牵张激活离子通道。
Am J Physiol. 1993 Mar;264(3 Pt 2):H960-72. doi: 10.1152/ajpheart.1993.264.3.H960.
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Novel cation-selective mechanosensitive ion channel in the atrial cell membrane.
Circ Res. 1993 Jan;72(1):225-31. doi: 10.1161/01.res.72.1.225.
10
A rapid and potent natriuretic response to intravenous injection of atrial myocardial extract in rats.大鼠静脉注射心房肌提取物后出现快速且强效的利钠反应。
Life Sci. 1981 Jan 5;28(1):89-94. doi: 10.1016/0024-3205(81)90370-2.

钆阻滞分离的大鼠心房中牵张激活的心房钠尿肽分泌。

Block of stretch-activated atrial natriuretic peptide secretion by gadolinium in isolated rat atrium.

作者信息

Laine M, Arjamaa O, Vuolteenaho O, Ruskoaho H, Weckström M

机构信息

Biocenter Oulu, Department of Physiology, University of Oulu, Finland.

出版信息

J Physiol. 1994 Nov 1;480 ( Pt 3)(Pt 3):553-61. doi: 10.1113/jphysiol.1994.sp020383.

DOI:10.1113/jphysiol.1994.sp020383
PMID:7869268
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1155828/
Abstract
  1. Isolated superfused rat atrial preparations were used to study the mechanism of stretch-induced atrial natriuretic peptide (ANP) secretion. The stretch of the atrial myocytes was induced by raising the intra-atrial pressure. The secretion rates were analysed by measuring ANP concentrations from the superfusate fractions by radioimmunoassay. 2. The effect of gadolinium, a blocker of stretch-activated ion channels, on stretch-induced and basal ANP secretion was investigated by superfusing the atrial preparation with 5, 20 or 80 microM GdCl3. Gadolinium decreased stretch-induced ANP secretion in a dose-dependent manner, but did not affect basal secretion. 3. Because high concentrations of gadolinium may block voltage-gated calcium channels, we tested whether the selective blockers of L-type (diltiazem) and T-type (NiCl2) calcium channels affect the stretch-stimulated ANP release. Neither diltiazem at 3 microM nor NiCl2 at 50 microM affected stretch-induced ANP release in paced atrial preparation. 4. Gadolinium, but not diltiazem, also inhibited stretch-stimulated ANP secretion in non-paced, quiescent atria. 5. The findings that ANP release is inhibited by Gd3+, but not by diltiazem or NiCl2, and that the stretch-induced secretion in quiescent atria is also inhibited by Gd3+, suggest that stretch-activated ion channels are involved in the regulation of stretch-induced ANP release.
摘要
  1. 采用离体灌流大鼠心房标本研究牵张诱导心房利钠肽(ANP)分泌的机制。通过升高心房内压诱导心房肌细胞牵张。通过放射免疫分析法测定灌流液组分中的ANP浓度来分析分泌率。2. 通过用5、20或80微摩尔/升的氯化钆灌流心房标本,研究了牵张激活离子通道阻滞剂钆对牵张诱导的和基础的ANP分泌的影响。钆以剂量依赖方式降低牵张诱导的ANP分泌,但不影响基础分泌。3. 由于高浓度的钆可能阻断电压门控钙通道,我们测试了L型(地尔硫䓬)和T型(氯化镍)钙通道的选择性阻滞剂是否影响牵张刺激的ANP释放。在起搏心房标本中,3微摩尔/升的地尔硫䓬和50微摩尔/升的氯化镍均不影响牵张诱导的ANP释放。4. 钆而非地尔硫䓬也抑制非起搏的静止心房中牵张刺激的ANP分泌。5. ANP释放受Gd3 +抑制而非地尔硫䓬或氯化镍抑制,以及静止心房中牵张诱导的分泌也受Gd3 +抑制,这些发现表明牵张激活离子通道参与牵张诱导的ANP释放的调节。