Wardle R L, Murphy R A
Department of Molecular Physiology and Biological Physics, University of Virginia Health Sciences Center, Charlottesville, Virginia 22906-0011, USA.
Am J Physiol. 1998 Oct;275(4):C1095-103. doi: 10.1152/ajpcell.1998.275.4.C1095.
Exposure of porcine carotid artery smooth muscle (PCASM) to histamine was followed by a large reduction in the rate of force generation in response to 40 mM KCl. This was shown to be a manifestation of slow attainment of a steady-state myoplasmic Ca2+ concentration ([Ca2+]i). We hypothesized that if net transsarcolemmal Ca2+ flux into the depolarized PCASM cells is the same before and after a desensitizing histamine treatment, then the transient attenuation of the increase in [Ca2+]i may be due to accelerated uptake of Ca2+ by a partially depleted sarcoplasmic reticulum (SR) acting as a Ca2+ sink or superficial buffer barrier. We tested this hypothesis by eliciting responses of "desensitized PCASM" to 40 mM KCl in the presence of cyclopiazonic acid (CPA), an SR Ca2+-ATPase inhibitor. Contractions of CPA-treated tissues were attenuated less than those of tissues not treated with CPA, but they were not abolished. CPA-insensitive mechanism(s) dominated the desensitization. We conclude that histamine pretreatment reduced net transsarcolemmal Ca2+ flux into PCASM in response to 40 mM KCl.
猪颈动脉平滑肌（PCASM）暴露于组胺后，对40 mM KCl产生的力量生成速率大幅降低。这被证明是肌浆Ca2+浓度（[Ca2+]i）达到稳态缓慢的一种表现。我们假设，如果在脱敏组胺处理前后，进入去极化PCASM细胞的跨肌膜Ca2+净通量相同，那么[Ca2+]i增加的短暂衰减可能是由于部分耗尽的肌浆网（SR）作为Ca2+汇或表面缓冲屏障加速摄取Ca2+所致。我们通过在存在环匹阿尼酸（CPA，一种SR Ca2+-ATP酶抑制剂）的情况下引发“脱敏PCASM”对40 mM KCl的反应来检验这一假设。CPA处理组织的收缩减弱程度小于未用CPA处理的组织，但并未完全消除。对CPA不敏感的机制主导了脱敏过程。我们得出结论，组胺预处理减少了PCASM对40 mM KCl的跨肌膜Ca2+净通量。
