Insulin attenuates vasopressin-induced calcium transients and a voltage-dependent calcium response in rat vascular smooth muscle cells.
Insulin attenuates vasopressin-induced calcium transients and a voltage-dependent calcium response in rat vascular smooth muscle cells.
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胰岛素可减弱大鼠血管平滑肌细胞中加压素诱导的钙瞬变和电压依赖性钙反应。
DOI：
10.1172/jci115426
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发表时间：
1991
期刊：
影响因子：
--
通讯作者：
Sowers,JR
中科院分区：
文献类型：
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作者：
Standley,PR;Zhang,F;Ram,JL;Zemel,MB;Sowers,JR
胰岛素减弱血管平滑肌 (VSM) 对各种激动剂的收缩反应。胰岛素缺乏和胰岛素抵抗大鼠缺乏血管收缩反应的正常减弱。为了研究这种减弱机制，研究了胰岛素对培养的 VSM 细胞 (a7r5) 对精氨酸加压素 (AVP) 的钙 (Ca2+) 反应和膜电位的影响。胰岛素（1 和 100 mU/ml）使 AVP 剂量反应曲线向右移动，使 AVP 的相对效力分别降低 16 倍和 220 倍。使用胰岛素后 30 分钟内，AVP 的反应显着减弱。 AVP 引起的 [Ca2+]i 升高部分依赖于细胞外 Ca2+。胰岛素治疗（100 mU/ml）90分钟后，AVP引起的内向电流减少，从-103 +/- 27 pA（正常）的峰值电流减少到-37 +/- 15 pA（胰岛素治疗）。峰值电压依赖性Ca(2+)依赖性内向电流不受胰岛素影响；然而，胰岛素使电流-电压曲线向右移动 16 +/-3 mV。因此，胰岛素可以通过减弱激动剂介导的 [Ca2+]i 升高来减少 VSM 收缩反应，而 [Ca2+]i 的升高部分是通过减少通过受体和电压操作通道的 Ca2+ 流入来介导的。
Insulin attenuates the contractile responses of vascular smooth muscle (VSM) to various agonists. Insulinopenic and insulin-resistant rats lack this normal attenuation of vascular contractile responses. To study this attenuating mechanism, the effects of insulin on calcium (Ca2+) responses of cultured VSM cells (a7r5) to arginine vasopressin (AVP) and membrane potential were investigated. Insulin (1 and 100 mU/ml) shifted AVP dose-response curves to the right, reducing relative potency of AVP by 16-fold and 220-fold, respectively. Responses to AVP were significantly attenuated within 30 min of insulin application. The AVP-elicited rise in [Ca2+]i was partially dependent upon extracellular Ca2+. AVP-elicited inward current was reduced by 90 min of insulin treatment (100 mU/ml), from a peak current of -103 +/- 27 pA (normal) to -37 +/- 15 pA (insulin treated). Peak voltage-dependent Ca(2+)-dependent inward current was unaffected by insulin; however, the current-voltage curve was shifted 16 +/-3 mV to the right by insulin. Thus, insulin may reduce VSM contractile responses by attenuating agonist-mediated rises in [Ca2+]i mediated, in part, by reductions in Ca2+ influx through both receptor- and voltage-operated channels.