Relative contributions of Ca2+ mobilization and influx in renal arteriolar contractile responses to arginine vasopressin.
Relative contributions of Ca2+ mobilization and influx in renal arteriolar contractile responses to arginine vasopressin.
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Ca2+ 动员和流入对精氨酸加压素肾小动脉收缩反应的相对贡献。
DOI：
10.1152/ajprenal.00150.2002
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发表时间：
2005
期刊：
影响因子：
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通讯作者：
Carmines,PamelaK
中科院分区：
文献类型：
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作者：
Fallet,RachelW;Ikenaga,Hideki;Bast,JosephP;Carmines,PamelaK
实验提出了这样的假设：传入和传出小动脉在产生对 AVP 的收缩反应时，不同程度地依赖 Ca2+ 流入和/或细胞内储备的释放。在来自大鼠肾脏的血液灌注的近髓肾单位中评估了 Ca2+ 储备耗尽或电压门控 Ca2+ 通道 (VGCC) 阻断对 AVP (0.01–1.0 nM) 收缩反应的影响。通过 100 μM 环吡桑酸 (CPA) 或 1 μM 毒胡萝卜素处理消除细胞内 Ca2+ 储备，分别使传入小动脉基线直径增加 14% 和 21%，但不会显着改变传出小动脉直径。 CPA 使传入和传出小动脉的收缩反应分别减弱 34% 和 55% 至 1.0 nM AVP（P= 0.013）。毒胡萝卜素对 AVP 诱导的传入小动脉收缩的影响（52% 抑制）也小于其对传出小动脉反应的影响（88% 抑制；P= 0.046）。在探索 Ca2+ 通过 VGCC 流入的作用的实验中，10 μM 地尔硫卓使基线传入小动脉直径增加 34%，并将收缩反应减弱到 1.0 nM AVP 45%，而不会显着改变传出小动脉基线直径或对 AVP 的反应性。地尔硫卓和毒胡萝卜素联合治疗可防止 AVP 诱导的两个血管段的收缩。我们得出的结论是，细胞内储存的 Ca2+ 释放有助于传入和传出小动脉对 AVP 的收缩反应，但在传出小动脉中更为突出。此外，VGCC 对 AVP 诱导的肾小动脉收缩的贡献主要在于传入小动脉。
Experiments addressed the hypothesis that afferent and efferent arterioles differentially rely on Ca2+influx and/or release from intracellular stores in generating contractile responses to AVP. The effect of Ca2+store depletion or voltage-gated Ca2+channel (VGCC) blockade on contractile responsiveness to AVP (0.01–1.0 nM) was assessed in blood-perfused juxtamedullary nephrons from rat kidney. Depletion of intracellular Ca2+stores by 100 μM cyclopiazonic acid (CPA) or 1 μM thapsigargin treatment increased afferent arteriolar baseline diameter by 14 and 21%, respectively, but did not significantly alter efferent arteriolar diameter. CPA attenuated the contractile response to 1.0 nM AVP by 34 and 55% in afferent and efferent arterioles, respectively (P= 0.013). The impact of thapsigargin on AVP-induced afferent arteriolar contraction (52% inhibition) was also less than its effect on the efferent arteriolar response (88% inhibition;P= 0.046). In experiments probing the role of the Ca2+influx through VGCCs, 10 μM diltiazem evoked a 34% increase in baseline afferent arteriolar diameter and attenuated the contractile response to 1.0 nM AVP by 45%, without significantly altering efferent arteriolar baseline diameter or responsiveness to AVP. Combined treatment with both diltiazem and thapsigargin prevented AVP-induced contraction of both vascular segments. We conclude that Ca2+release from the intracellular stores contributes to the contractile response to AVP in both afferent and efferent arterioles but is more prominent in the efferent arteriole. Moreover, the VGCC contribution to AVP-induced renal arteriolar contraction resides primarily in the afferent arteriole.