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首页> 外文期刊>American Journal of Physiology >Src family kinase involvement in rat preglomerular microvascular contractile and (Ca2+)i responses to ANG II.
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Src family kinase involvement in rat preglomerular microvascular contractile and (Ca2+)i responses to ANG II.

机译：Src家族激酶参与大鼠肾小球前微血管收缩和对ANG II的（Ca2 +）i反应。

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摘要

Experiments were performed to investigate the potential role of Src family kinase(s) in the rat afferent arteriolar contractile response to ANG II. The in vitro blood-perfused juxtamedullary nephron technique was employed to monitor afferent arteriolar lumen diameter responses to 1-100 nM ANG II before and during Src family kinase inhibition (10 microM PP2). PP2 did not alter baseline diameter but attenuated ANG II-induced contractile responses by 33 +/- 6%. An inactive analog of PP2 (PP3) had no effect on ANG II-induced afferent arteriolar contraction. The effect of Src kinase inhibition on ANG II-induced intracellular free Ca(2+) concentration ([Ca(2+)](i)) responses was probed in fura 2-loaded preglomerular microvascular smooth muscle cells (PVSMCs) obtained from explants and studied after 3-5 days in culture. In untreated PVSMCs, ANG II evoked peak (Delta = 293 +/- 66 nM) and plateau (Delta = 23 +/- 8 nM) increases in [Ca(2+)](i). In PVSMCs pretreated with PP2, baseline [Ca(2+)](i) was unaltered, but both the peak (Delta = 140 +/- 22 nM) and plateau (Delta = 3 +/- 2 nM) phases of the ANG II response were significantly reduced compared with untreated cells. PP3 did not alter [Ca(2+)](i) responses to ANG II. Immunoprecipitation and Western blot analysis confirmed that 100 nM ANG II increased phosphorylation of c-Src (at Y(416)) in PVSMCs. The phosphorylation response was maximal 1 min after ANG II exposure and was prevented by PP2. We conclude that the preglomerular vasoconstriction evoked by ANG II involves rapid c-Src activation with subsequent effects that contribute to the [Ca(2+)](i) response to the peptide.
机译：进行实验以研究Src家族激酶在大鼠对ANG II的小动脉收缩反应中的潜在作用。在Src家族激酶抑制（10 microM PP2）之前和期间，采用体外血液灌注近髓肾单位技术来监测对1-100 nM ANG II的传入小动脉腔直径反应。 PP2不会改变基线直径，但会使ANG II诱导的收缩反应减弱33 +/- 6％。 PP2（PP3）的非活性类似物对ANG II诱导的传入小动脉收缩没有影响。 Src激酶抑制作用对ANG II诱导的细胞内游离Ca（2+）浓度（[Ca（2 +）]（i））响应的影响从外植体中获得的呋喃2加载的肾小球前微血管平滑肌细胞（PVSMC）并在培养3-5天后进行研究。在未经处理的PVSMC中，ANG II引起的峰值（Delta = 293 +/- 66 nM）和平稳期（Delta = 23 +/- 8 nM）在[Ca（2 +）]（i）中增加。在PP2预处理的PVSMC中，基线[Ca（2 +）]（i）不变，但是ANG的峰相（Delta = 140 +/- 22 nM）和平稳期（Delta = 3 +/- 2 nM）与未处理的细胞相比，II反应显着降低。 PP3不会改变对ANG II的[Ca（2 +）]（i）反应。免疫沉淀和Western印迹分析证实100 nM ANG II增加了PVSMC中c-Src的磷酸化（位于Y（416））。 ANG II暴露后磷酸化反应最大1分钟，并被PP2阻止。我们得出的结论是由ANG II引起的肾小球前血管收缩涉及快速c-Src激活以及随后的作用，这些作用有助于对肽的[Ca（2 +）]（i）反应。

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