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链霉素对大鼠脑动脉肌源性张力、钾离子诱导的收缩力及L型钙电流的抑制作用。

Streptomycin inhibition of myogenic tone, K+-induced force and block of L-type calcium current in rat cerebral arteries.

作者信息

Miller A L, Langton P D

机构信息

Department of Physiology, University of Bristol, University Walk, Bristol BS8 1TD, UK.

出版信息

J Physiol. 1998 May 1;508 ( Pt 3)(Pt 3):793-800. doi: 10.1111/j.1469-7793.1998.793bp.x.

Abstract
  1. Streptomycin has been demonstrated to inhibit mechanosensitive conductances in a wide variety of cell types, including muscle. The action of streptomycin on rat cerebral arteries that exhibit pressure-induced myogenic response was investigated. 2. Pressure-induced tone, measured using isobaric myography, in isolated pressurized cerebral arteries was reversibly and concentration-dependently inhibited by streptomycin with an IC50 of 2.6 mM. 3. Isometric K+-induced force, measured using isometric myography, is supported by voltage-gated Ca2+ entry. Streptomycin reversibly and concentration-dependently inhibited isometric force with an IC50 of 1.71 mM. 4. Voltage-gated macroscopic inward Ca2+ channel currents were recorded from freshly isolated rat basilar myocytes. These were reversibly and concentration-dependently inhibited by streptomycin with an IC50 of 1.79 and 0.47 mM when 10 and 1.8 mM CaCl2, respectively, was used as the charge carrier. 5. These data suggest that streptomycin inhibits myogenic tone and K+-induced isometric force largely by blockade of L-type, dihydropyridine-sensitive Ca2+ channels. In conclusion, streptomycin is not useful in the investigation of stretch-activated channels which may underlie the myogenic response of rat small cerebral arteries.
摘要
  1. 链霉素已被证明能抑制多种细胞类型(包括肌肉细胞)中的机械敏感电导。研究了链霉素对表现出压力诱导肌源性反应的大鼠脑动脉的作用。2. 使用等压肌动描记法测量,链霉素可使离体加压脑动脉中压力诱导的张力可逆且浓度依赖性地受到抑制,半数抑制浓度(IC50)为2.6 mM。3. 使用等长肌动描记法测量,等长钾离子诱导的力由电压门控钙内流支持。链霉素可逆且浓度依赖性地抑制等长力,IC50为1.71 mM。4. 从新鲜分离的大鼠基底肌细胞记录电压门控宏观内向钙通道电流。当分别使用10 mM和1.8 mM氯化钙作为载流子时,这些电流被链霉素可逆且浓度依赖性地抑制,IC50分别为1.79 mM和0.47 mM。5. 这些数据表明,链霉素主要通过阻断L型、对二氢吡啶敏感的钙通道来抑制肌源性张力和钾离子诱导的等长力。总之,链霉素在研究可能是大鼠小脑动脉肌源性反应基础的牵张激活通道方面并无用处。

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