Vessel- and target cell-specific actions of endothelin-1 and endothelin-3 in rat liver.

Vessel- and target cell-specific actions of endothelin-1 and endothelin-3 in rat liver.
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内皮素 1 和内皮素 3 在大鼠肝脏中的血管和靶细胞特异性作用。

DOI:
10.1152/ajpgi.1995.269.2.g269
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发表时间:
1995
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Clemens,MG
Clemens,MG
中科院分区:
--
文献类型:
--
作者:
Zhang,JX;Bauer,M;Clemens,MG

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被引文献

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我们研究了肝微循环对内皮素-1(ET-1)和内皮素-3(ET-3)的窦状和窦外收缩反应,以及Ito细胞与枯否细胞或内皮细胞在介导这种反应中的可能作用。通过静脉内注射2.6 × 10(8)荧光乳胶珠(1微米)对大鼠进行预处理以标记枯否细胞。3小时后,在输注1 nM ET-1或ET-3(有或没有内皮素A型(ETA)受体拮抗剂BQ-123或ETB拮抗剂IRL-1038)之前和期间分离肝脏并灌注。或者,用ETB激动剂sarafotoxin 6c(S6 c,1或5 nM)输注灌注的肝脏。在Ito细胞(通过维生素A荧光鉴定)或Kupffer细胞(吞噬荧光乳胶珠)或未发现细胞类型(内皮细胞)的部位定量窦状隙直径。ET-1可使Ito细胞窦状隙明显收缩(对照组为13.21 +/- 0.58微米,ET-1输注期间为10.47 +/- 0.48微米),但在枯否细胞或内皮细胞部位未观察到(分别为13.26 +/- 0.79对12.92 +/- 0.61微米和12.20 +/- 0.71对11.98 +/- 0.40微米),而ET-3和S6 c对窦状隙变窄均无任何影响,尽管与ET-1相比,总门静脉阻力增加了1.8倍(ET-3)或5.6倍(5 nM S6 c)。(250字处删节)
We studied the sinusoidal and extrasinusoidal constrictor response of hepatic microcirculation to endothelin-1 (ET-1) and endothelin-3 (ET-3) and the possible role of Ito cells vs. Kupffer cells or endothelial cells in mediating this response, using isolated rat livers under high-power intravital microscopy. Rats were pretreated by injection of 2.6 x 10(8) fluorescent latex beads (1 micron) intravenously to label Kupffer cells. Three hours later livers were isolated and perfused before and during the infusion of 1 nM ET-1 or ET-3 with or without the endothelin type A (ETA) receptor antagonist BQ-123 or ETB antagonist IRL-1038. Alternatively, the perfused livers were infused with the ETB agonist sarafotoxin 6c (S6c, 1 or 5 nM). Sinusoid diameters were quantitated at the sites of Ito cells (identified by vitamin A fluorescence) or Kupffer cells (phagocytosed fluorescent latex beads) or where neither cell type was found (endothelial cells). ET-1 was found to induce significant sinusoid constriction at the sites of Ito cells (13.21 +/- 0.58 microns control vs. 10.47 +/- 0.48 microns during ET-1 infusion) but not at the sites of Kupffer cells or endothelial cells (13.26 +/- 0.79 vs. 12.92 +/- 0.61 microns and 12.20 +/- 0.71 vs. 11.98 +/- 0.40 microns, respectively), whereas neither ET-3 nor S6c had any effect on sinusoid narrowing, despite a 1.8-fold (ET-3) or 5.6-fold (5 nM S6c) greater increase in total portal resistance compared with ET-1.(ABSTRACT TRUNCATED AT 250 WORDS)