Suppr超能文献

体外分离灌流的蜗轴螺旋动脉中血管张力和收缩性的钙离子依赖性及硝苯地平敏感性

Ca2+-dependence and nifedipine-sensitivity of vascular tone and contractility in the isolated superfused spiral modiolar artery in vitro.

作者信息

Wangemann P, Cohn E S, Gruber D D, Gratton M A

机构信息

Cell Physiology Laboratory, Boys Town National Research Hospital, Omaha, NE 68131, USA.

出版信息

Hear Res. 1998 Apr;118(1-2):90-100. doi: 10.1016/s0378-5955(98)00017-3.

Abstract

The regulation of the vascular diameter of the spiral modiolar artery may play a major role in the regulation of cochlear blood flow and tissue oxygenation since the spiral modiolar artery provides the main blood supply to the cochlea. The goal of the present study was to determine whether vascular tone and contractility of the spiral modiolar artery depend on the presence of extracellular Ca2+ and involves nifedipine-sensitive Ca2+ channels. The spiral modiolar artery was isolated and superfused in vitro and the diameter was measured continuously by video microscopy. Isolated segments of the spiral modiolar artery had an outer diameter of 61 +/- 3 microm (n = 59) and displayed vasomotion characterized by 5-15 clearly distinguishable constrictions per min. Removal of Ca2+ from the superfusion medium caused a reversible relaxation and cessation of vasomotion and was used to determine the magnitude of basal vascular tone. The basal vascular tone consisted of a sustained reduction of the vascular diameter to 95.1 +/- 0.3% (n = 51) of the maximal diameter in Ca2+-free medium. Nifedipine reduced the basal vascular tone with an IC50 of (1.1 +/- 0.3) x 10(-9)) M although 22% of the basal vascular tone was insensitive to nifedipine. Elevation of the K+ concentration from 3.6 to 150 mM caused a transient vasoconstriction which was dependent on the presence of extracellular Ca2+. Nifedipine fully inhibited K+-induced vasoconstriction with an IC50 of (2.0 +/- 0.7) x 10(-9) M. Norepinephrine (10(-4) M) caused a transient vasoconstriction and an increase of vasomotion at branch points of the spiral modiolar artery. Norepinephrine-induced vasoconstriction was fully inhibited in the absence of Ca2+ and partially inhibited by 10(-7) M nifedipine. These observations suggest that the spiral modiolar artery contains voltage-dependent nifedipine-sensitive Ca2+ channels which are involved in the maintenance of basal vascular tone as well as in the mediation of K+- and norepinephrine-induced contractility. Further, the data suggest that cytosolic Ca2+ stores, if present in the spiral modiolar artery, are of limited capacity compared to other vessels.

摘要

由于螺旋蜗轴动脉是耳蜗的主要血液供应来源,其血管直径的调节可能在耳蜗血流和组织氧合的调节中起主要作用。本研究的目的是确定螺旋蜗轴动脉的血管张力和收缩性是否依赖于细胞外Ca2+的存在,并涉及硝苯地平敏感的Ca2+通道。将螺旋蜗轴动脉分离并在体外进行灌流,通过视频显微镜连续测量其直径。分离的螺旋蜗轴动脉段外径为61±3微米(n = 59),表现出血管运动,其特征为每分钟有5 - 15次明显可辨的收缩。从灌流培养基中去除Ca2+会导致可逆的舒张和血管运动停止,并用于确定基础血管张力的大小。基础血管张力包括血管直径持续减小至无Ca2+培养基中最大直径的95.1±0.3%(n = 51)。硝苯地平降低基础血管张力,IC50为(1.1±0.3)×10(-9) M,尽管22%的基础血管张力对硝苯地平不敏感。将K+浓度从3.6 mM提高到150 mM会引起短暂的血管收缩,这依赖于细胞外Ca2+的存在。硝苯地平以IC50为(2.0±0.7)×10(-9) M完全抑制K+诱导的血管收缩。去甲肾上腺素(10(-4) M)会引起短暂的血管收缩,并使螺旋蜗轴动脉分支点处的血管运动增加。在无Ca2+的情况下,去甲肾上腺素诱导的血管收缩被完全抑制,而10(-7) M硝苯地平可部分抑制。这些观察结果表明,螺旋蜗轴动脉含有电压依赖性的硝苯地平敏感Ca2+通道,这些通道参与基础血管张力的维持以及K+和去甲肾上腺素诱导的收缩性的介导。此外,数据表明,螺旋蜗轴动脉中如果存在胞质Ca2+储存,其容量与其他血管相比有限。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验